Pubmed	Chromosome	Start_position	End_position	Enhancer_related_genes	Description	Species	Tissue_class	Experiment_class	Title	SNP_related	SNP_id	Disease	Cell_class	Enhancer_id	Enhancer_experiment	Enhancer_tar_ex_De	Enhancer_type	target_gene_strong_experiment	target_gene_weak_experiment	target_gene_experiment_description	target_gene_other_name	Enhancer_function	Enhancer_function_experiment	En_function_ex_de	TF_name	TF_other_name	Experiment	TF_experiment_de	SNP_position	SNP_experiment	Target_gene
29364907	chr2	28389994	28391994	FOSL2	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	human	Cervix	High+Lowthroughput	HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression	否		HPV positive tumors	cervical-derived cell line 20861	E_01_0001	Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	Immunohistochemical staining	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	FOSL2		Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.			
29364907	chr17	32412637	32414637	Brd4	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA	mouse	Cervix	High+Lowthroughput	HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression	否		HPV positive tumors	cervical-derived cell line 20861	E_01_0001	Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA		ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA	Immunohistochemical staining	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA			Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH				Brd4
29363938	chr2	207527779	207529779	CREB1	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	human	Cervix	High+Lowthroughput	Universal mRNA Translation Enhancement with Gold Nanoparticles Conjugated to Oligonucleotides with a Poly(T) Sequence	否		cervical cancer	HeLa cell	E_01_0002	Western blot,RT-PCR,PCR	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	Immunohistochemical staining	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	CREB1		Western blot,RT-PCR,PCR	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.			
29363553	chr6	47503992	47505992	Ezh2	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	mouse	Bone marrow	High+Lowthroughput	Hematopoietic stem/progenitor cell senescence is associated with altered expression profiles of cellular memory-involved gene	否	Enhancer_experiment	senescence associated disease	progenitor cell	E_02_0001	qRT-PCR	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.		Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Immunohistochemical staining	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.			qRT-PCR				Ezh2
29358714	chr15	58585627	58587627	ADAM10	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.	human,mouse	Nerve	High+Lowthroughput	Identification of disulfiram as a secretase-modulating compound with beneficial effects on Alzheimer's disease hallmarks	否		Alzheimer’s disease	SH-SY5Y human neuronal cell	E_02_0002	Western blot,RT-PCR	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.		ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.	Immunohistochemical staining	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.			Western blot,RT-PCR				ADAM10
29358650	chr4	139461205	139463205	Pax7	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.	mouse	Hypophysoma	High+Lowthroughput	Pioneer factor Pax7 deploys a stable enhancer repertoire for specification of cell fate	否		Hypophysoma	AtT-20 cell	E_02_0003	ChIP–seq,ATAC–seq,RNA-seq	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.		Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.	Immunohistochemical staining	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.			ChIP–seq,ATAC–seq,RNA-seq				Pax7
29357419	chr7	148804764	148806764	EZH2	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	human	Kidney	High+Lowthroughput	Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu	否		kidney disease	epithelial cell	E_01_0003	Western blot,Immunofluorescence,Transfection	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	Immunohistochemical staining	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	EZH2		Western blot,Immunofluorescence,Transfection	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2			
29344674	chr7	148805135	148807135	EZH2	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	human	Oral cavity	High+Lowthroughput	Long non-coding RNA H1 promotes cell proliferation and invasion by acting as a ceRNA of miR?138 and releasing EZH2 in oral squamous cell carcinoma	否		oral squamous cell carcinoma	oral squamous cell carcinoma cell	E_01_0004	RT-qPCR,transfection,Western blot	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	Immunohistochemical staining	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	EZH2		RT-qPCR,transfection,Western blot	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.			
29344090	chr12	102954386	102956386	ASCL1	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	human	Bone marrow and lymphatic tissue	High+Lowthroughput	Overexpression of the proneural transcription factor ASCL1 in chronic lymphocytic leukemia with a t(12;14)(q23.2;q32.3)	否		chronic lymphocytic leukemia	chronic lymphocytic leukemia cell	E_01_0005	qPCR,FISH	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	Immunohistochemical staining	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	ASCL1		qPCR,FISH	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.			
29344006	chr6	113930322	113932322	HDAC2	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.	human	Connective tissue	High+Lowthroughput	Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression	否		Sepsis	macrophage	E_01_0006	ChIP,qRT-PCR,Western blot	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.		HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.	Immunohistochemical staining	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.			ChIP,qRT-PCR,Western blot				HDAC2
29344006	chr6	31572978	31574978	TNF	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	human	Connective tissue	High+Lowthroughput	Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression	否		Sepsis	macrophage	E_01_0006	ChIP,qRT-PCR,Western blot	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	Immunohistochemical staining	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	TNF		ChIP,qRT-PCR,Western blot	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.			
29343853	chr7	78700257	78702257	Acan	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood	mouse	Cartilage tissue	High+Lowthroughput	Differential tissue specific, temporal and spatial expression patterns of the Aggrecan gene is modulated by independent enhancer elements	否		In debilitating diseases such as osteoarthritis, where increased mechanical stress on chondrocytes.	chondroblast	E_02_0004	Western blot	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood		Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood	Immunohistochemical staining	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood			Western blot				Acan
29343853	chr17	72118279	72120279	SOX9	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	human	Cartilage tissue	High+Lowthroughput	Differential tissue specific, temporal and spatial expression patterns of the Aggrecan gene is modulated by independent enhancer elements	否		In debilitating diseases such as osteoarthritis, where increased mechanical stress on chondrocytes.	chondroblast	E_02_0004	Western blot	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	Immunohistochemical staining	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	SOX9		Western blot	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.			
29343500	chr9	123505056	123507056	Ccr9	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.	mouse	Thymus	High+Lowthroughput	Cbfβ2 controls differentiation of and confers homing capacity to prethymic progenitors	否		thymus homing	thymocyte	E_02_0005	Western blot,ChIP-seq,RNA-seq	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.		Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.	Immunohistochemical staining	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.			Western blot,ChIP-seq,RNA-seq				Ccr9
29343500	chr8	105894833	105896833	Cbfb	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.	mouse	Thymus	High+Lowthroughput	Cbfβ2 controls differentiation of and confers homing capacity to prethymic progenitors	否		thymus homing	thymocyte	E_02_0005	Western blot,ChIP-seq,RNA-seq	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.		Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.	Immunohistochemical staining	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.			Western blot,ChIP-seq,RNA-seq				Cbfb
29343483	chr7	34815932	34817932	Cebpa	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.	mouse	Bone marrow	High+Lowthroughput	NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling	否		myelodysplastic disease	hematopoietic stem cell	E_02_0006	RT-qPCR	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.		Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.	Immunohistochemical staining	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.			RT-qPCR				Cebpa
29343483	chr12	52019947	52021947	NR4A1	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	human,mouse	Bone marrow	High+Lowthroughput	NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling	否		myelodysplastic disease	hematopoietic stem cell	E_02_0006	RT-qPCR	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses		Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Immunohistochemical staining	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses			RT-qPCR				NR4A1
29343483	chr9	99818517	99820517	NR4A3	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	human,mouse	Bone marrow	High+Lowthroughput	NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling	否		myelodysplastic disease	hematopoietic stem cell	E_02_0006	RT-qPCR	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses		Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Immunohistochemical staining	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses			RT-qPCR				NR4A3
29343442	chr12	57092345	57094345	STAT6	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.	human,mouse	Bone marrow	High+Lowthroughput	The Transcription Factor STAT6 Mediates Direct Repression of Inflammatory Enhancers and Limits Activation of Alternatively Polarized Macrophages	否		inflammatory diseases	macrophage	E_02_0007	ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.		Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.	Immunohistochemical staining	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.			ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR				STAT6
29343442	chr5	141618696	141620696	HDAC3	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes	human,mouse	Bone marrow	High+Lowthroughput	The Transcription Factor STAT6 Mediates Direct Repression of Inflammatory Enhancers and Limits Activation of Alternatively Polarized Macrophages	否		ainflammatory diseases	macrophage	E_02_0007	ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes		The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes	Immunohistochemical staining	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes			ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR				HDAC3
29342503	chr5	173229371	173231371	NKX2-5	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0007	Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Immunohistochemical staining	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	NKX2-5		Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.			
29342503	chr11	12671461	12673461	TEAD1	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0007	Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Immunohistochemical staining	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	TEAD1		Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease			
29342133	chr15	63714919	63952099	Myc	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	mouse	Haematopoietic tissue	Low+High throughput	A Myc enhancer cluster regulates normal and leukaemic haematopoietic stem cell hierarchies	否	--	Leukaemia	hematopoietic stem cell	E_02_0008	ChIP-seq	Here we show that an evolutionarily conserved region located 1.7 megabases downstream of the Myc gene that has previously been labelled as a ‘super_x0002_enhancer’2 is essential for the regulation of Myc expression levels in both normal haematopoietic and leukaemic stem cell hierarchies in mice and humans. Deletion of this region in mice leads to a complete loss of Myc expression in haematopoietic stem cells and progenitors.	Super-Enhancer	--	ChIP-seq,ATAC-seq,RT-qPCR	In line with this hypothesis, chromatin conformation capture performedon mouse leukaemic cells2 as well as DNA proximity analysis using fluorescence in situ hybridization (DNA FISH) in LSK cells showed that the Myc promoter and BENC are in close physical proximity to each other, suggesting that cis-regulation is mediated by chromosomal looping in haematopoietic stem and progenitor cells.	AU0167572,Niard,Nird,bHLHe39,?Myc	Clusters of enhancers, such as BENC, form highly combinatorial systems that allow precise control of gene expression across normal cellular hierarchies and which also can be hijacked in malignancies.	ATAC-seq,RT-qPCR	Analysis of mice carrying deletions of individual Enhancer modules suggests that specific Myc expression levels throughout most of the haematopoietic hierarchy are controlled by the combinatorial and additive activity of individual Enhancer modules, which collectively function as a ‘blood Enhancer cluster’(BENC).	--	--	--	--	--	--	Myc
29339538	chr7	55016139	55018139	EGFR	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	human	Cervix	High+Lowthroughput	E6 Protein Expressed by High-Risk HPV Activates Super-Enhancers of the EGFR and c-MET Oncogenes by Destabilizing the Histone Demethylase KDM5C	否		human papillomaviruses	CaSki cell(human cervical cancer cell line)	E_01_0008	ChIP-seq,RNA-seq	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	Immunohistochemical staining	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	EGFR		ChIP-seq,RNA-seq	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.			
29339538	chrX	53173366	53175366	KDM5C	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	human	Cervix	High+Lowthroughput	E6 Protein Expressed by High-Risk HPV Activates Super-Enhancers of the EGFR and c-MET Oncogenes by Destabilizing the Histone Demethylase KDM5C	否		human papillomaviruses	CaSki cell(human cervical cancer cell line)	E_01_0008	ChIP-seq,RNA-seq	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	Immunohistochemical staining	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	KDM5C		ChIP-seq,RNA-seq	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.			
29339121	chr8	144288666	144290666	HSF1	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	human	Gastric cancer tissues	High+Lowthroughput	HSF1, in association with MORC2, downregulates ArgBP2 via the PRC2 family in gastric cancer cells	否		gastric cancer	gastric cancer cell	E_01_0009	ChIP,Real-time PCR,Western blot	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	Immunohistochemical staining	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	HSF1		ChIP,Real-time PCR,Western blot	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.			
29339121	chr7	148804519	148806519	EZH2	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	human	Gastric cancer tissues	High+Lowthroughput	HSF1, in association with MORC2, downregulates ArgBP2 via the PRC2 family in gastric cancer cells	否		gastric cancer	gastric cancer cell	E_01_0009	ChIP,Real-time PCR,Western blot	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	Immunohistochemical staining	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	EZH2		ChIP,Real-time PCR,Western blot	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED			
29339121	chr22	30922434	30924434	MORC2	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2	human	Gastric cancer tissues	High+Lowthroughput	HSF1, in association with MORC2, downregulates ArgBP2 via the PRC2 family in gastric cancer cells	否		gastric cancer	gastric cancer cell	E_01_0009	ChIP,Real-time PCR,Western blot	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2		In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2	Immunohistochemical staining	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2			ChIP,Real-time PCR,Western blot				MORC2
29337370	chr16	28929378	28931378	CD19	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	human	Lymphoid tissue bone marrow	High+Lowthroughput	Modulating Gene Expression in Epstein-Barr Virus (EBV)-Positive B Cell Lines with CRISPRa and CRISPRi	否		Epstein-Barr virus	B cell	E_01_0010	ChIP-seq,ChIA-PET,RT-PCR	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).		GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Immunohistochemical staining	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).			ChIP-seq,ChIA-PET,RT-PCR				CD19
29337370	chr3	122052540	122054540	CD86	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	human	Lymphoid tissue bone marrow	High+Lowthroughput	Modulating Gene Expression in Epstein-Barr Virus (EBV)-Positive B Cell Lines with CRISPRa and CRISPRi	否		Epstein-Barr virus	B cell	E_01_0010	ChIP-seq,ChIA-PET,RT-PCR	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Immunohistochemical staining	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	CD86		ChIP-seq,ChIA-PET,RT-PCR	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).			
29334376	chr1	94526560	94528560	F3	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.	human	Osteosarcoma	High+Lowthroughput	Positively selected enhancer elements endow osteosarcoma cells with metastatic competence	否		Osteosarcoma	osteosarcoma cell	E_01_0011	RNA-seq,ChIP–seq	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.		We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.	Immunohistochemical staining	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.			RNA-seq,ChIP–seq				F3
29331299	chr16	29880720	29882720	Hes1	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton	human,mouse	Bone	High+Lowthroughput	The regulatory roles of Notch in osteocyte differentiation via the crosstalk with canonical Wnt pathways during the transition of osteoblasts to osteocytes	否			osteocyte	E_02_0009	RT-qPCR,Western blot, transfection, Immunofluorescence	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton		During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton	Immunohistochemical staining	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton			RT-qPCR,Western blot, transfection, Immunofluorescence				Hes1
29331016	chr10	112947442	112949442	TCF7L2	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	human	Liver	High+Lowthroughput	A candidate functional SNP rs7074440 in TCF7L2 alters gene expression through C-FOS in hepatocytes	是	rs7903146	type 2 diabetes	hepatocyte	E_01_0012	qRT-PCR,ChIP,Transfection	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	Immunohistochemical staining	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	TCF7L2		qRT-PCR,ChIP,Transfection	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.			
29327713	chr7	148804434	148806434	EZH2	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	human	Lymphoid tissue	High+Lowthroughput	Expression of enhancer of zeste homolog 2 (EZH2) protein in histiocytic and dendritic cell neoplasms with evidence for p-ERK1/2-related, but not MYC- or p-STAT3-related cell signaling	否		histiocytic and dendritic cell neoplasms	histiocytic and dendritic cell neoplasm cell	E_01_0013	Immunohistochemical staining	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	Immunohistochemical staining	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	EZH2		Immunohistochemical staining	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.			
29325110	chr5	56096484	56098484	ANKRD55	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.	human	Lymphoid tissue	High+Lowthroughput	Impact of genetic risk loci for multiple sclerosis on expression of proximal genes in patients	是	rs71624119	multiple sclerosis	peripheral blood mononuclear cell	E_01_0014	RNA-Seq	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.		As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.	Immunohistochemical staining	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.			RNA-Seq				ANKRD55
29323272	chr19	10958350	10960350	SMARCA4	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	human	Tumor	High+Lowthroughput	Dominant-negative SMARCA4 mutants alter the accessibility landscape of tissue-unrestricted enhancers	否		Tumor	embryonic stem cell	E_01_0015	Western blot,ATAC-seq,ChIP-seq,RNA-seq	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	Immunohistochemical staining	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	SMARCA4		Western blot,ATAC-seq,ChIP-seq,RNA-seq	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.			
29321660	chr3	186043535	186045535	ETV5	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	human,mouse	Neuroblastoma	High+Lowthroughput	Activated ALK signals through the ERK-ETV5-RET pathway to drive neuroblastoma oncogenesis	否		neuroblastoma	neuroblastoma cell lines	E_02_0010	ChIP-seq,RT-qPCR	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.		Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Immunohistochemical staining	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.			ChIP-seq,RT-qPCR				ETV5
29321660	chr10	43074431	43076431	RET	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	human,mouse	Neuroblastoma	High+Lowthroughput	Activated ALK signals through the ERK-ETV5-RET pathway to drive neuroblastoma oncogenesis	否		neuroblastoma	neuroblastoma cell lines	E_02_0010	ChIP-seq,RT-qPCR	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.		Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Immunohistochemical staining	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.			ChIP-seq,RT-qPCR				RET
29321583	chr3	34155732	34157732	Sox2ot	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.	mouse	Embryo	High+Lowthroughput	Allele-specific repression of Sox2 through the long non-coding RNA Sox2ot	否			embryonic stem cell	E_02_0011	qRT-PCR,qPCR,ChIP,3C	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.		Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.	Immunohistochemical staining	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.			qRT-PCR,qPCR,ChIP,3C				Sox2ot
29321583	chr3	34702062	34704062	Sox2	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.	mouse	Embryo	High+Lowthroughput	Allele-specific repression of Sox2 through the long non-coding RNA Sox2ot	否			embryonic stem cell	E_02_0011	qRT-PCR,qPCR,ChIP,3C	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.		The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.	Immunohistochemical staining	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.			qRT-PCR,qPCR,ChIP,3C				Sox2
29320736	chr15	41514637	41516637	RPAP1	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.	human,mouse	Connective tissue	High+Lowthroughput	The RNA Polymerase II Factor RPAP1 Is Critical for Mediator-Driven Transcription and Cell Identity	否		maintaining cell identity	stem cell	E_02_0012	ChIP-qPCR,ChIP-Seq,RNA-Seq,qRT-PCR	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.		We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.	Immunohistochemical staining	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.			ChIP-qPCR,ChIP-Seq,RNA-Seq,qRT-PCR				RPAP1
29320702	chr1	3066690	3068690	PRDM16	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	human,mouse	Adipose Tissue	High+Lowthroughput	Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis	否		obesity or type 2 diabetes	fat cell	E_02_0013	RNA-Seq,ChIP	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.		These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Immunohistochemical staining	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.			RNA-Seq,ChIP				PRDM16
29320702	chr7	74450980	74452980	GTF2IRD1	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	human,mouse	Adipose Tissue	High+Lowthroughput	Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis	否		obesity or type 2 diabetes	fat cell	E_02_0013	RNA-Seq,ChIP	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.		These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Immunohistochemical staining	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.			RNA-Seq,ChIP				GTF2IRD1
29320702	chr9	137616279	137618279	EHMT1	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	human,mouse	Adipose Tissue	High+Lowthroughput	Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis	否		obesity or type 2 diabetes	fat cell	E_02_0013	RNA-Seq,ChIP	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.		These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Immunohistochemical staining	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.			RNA-Seq,ChIP				EHMT1
29316219	chr9	81580914	81582914	TLE1	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	human	Brain	High+Lowthroughput	Characterization of a FOXG1:TLE1 transcriptional network in glioblastoma-initiating cells	否		Glioblastoma	glioblastoma-initiating cells	E_01_0016	ChIP-Seq,RNA-Seq,RT-qPCR	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	Immunohistochemical staining	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	TLE1		ChIP-Seq,RNA-Seq,RT-qPCR	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.			
29311615	chr12	54030827	54032827	HOXC5	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	human	Somatic tissue	High+Lowthroughput	HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis	否		Tumor	somatic cell	E_01_0017	Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Immunohistochemical staining	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	HOXC5		Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.			
29309299	chr19	19143072	19145072	MEF2B	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	human	Lymphoid tissue	High+Lowthroughput	Comparison of Myocyte Enhancer Factor 2B Versus Other Germinal Center-associated Antigens in the Differential Diagnosis of B-Cell Non-Hodgkin Lymphomas	否		Lymphomas	B cell	E_01_0018	Immunohistochemical Staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.		Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Immunohistochemical staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.			Immunohistochemical Staining				MEF2B
29307778	chr17	43750876	43752876	SOST	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	human	Bone	High+Lowthroughput	Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis	是	rs1230399, rs7220711, rs1107748, rs75901553	osteoporosis	Germinal center B-cells	E_01_0019	Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.		The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Immunohistochemical staining	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.			Luciferase reporter assay,ChIP,qPCR				SOST
29307778	chr16	67559199	67561199	CTCF	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	human	Bone	High+Lowthroughput	Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis	是	rs1230399, rs7220711, rs1107748, rs75901553	osteoporosis	Germinal center B-cells	E_01_0019	Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Immunohistochemical staining	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	CTCF		Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.			
29304378	chr6	151654024	151656024	ESR1	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	human	Bone	High+Lowthroughput	Life-Course Genome-wide Association Study Meta-analysis of Total Body BMD and Assessment of Age-Specific Effects	是	rs2982562-C	osteoporosis	osteocyte	E_01_0020	Knockout	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	Immunohistochemical staining	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	ESR1		Knockout	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.			
29303507	chr11	68036369	68038369	TCIRG1	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.	human	HCC tissue	High+Lowthroughput	T-cell immune regulator 1 enhances metastasis in hepatocellular carcinoma	否		hepatocellular carcinoma	HCC cell lines	E_01_0021	Western blot,transfection	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.		These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.	Immunohistochemical staining	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.			Western blot,transfection				TCIRG1
29302059	chr1	133246792	133248792	Kiss1	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.	human,mouse	Hypothalamic tissue	High+Lowthroughput	Trithorax dependent changes in chromatin landscape at enhancer and promoter regions drive female puberty	否		female puberty	Automatic Recognition of Cells	E_02_0014	qPCR,RNA-seq,ChIP	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.		Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.	Immunohistochemical staining	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.			qPCR,RNA-seq,ChIP				Kiss1
29301908	chr6	6874986	6876986	Dlx5	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	mouse	Inner ear	High+Lowthroughput	Deletion of a Long-Range Dlx5 Enhancer Disrupts Inner Ear Development in Mice	否		inner ear dysmorphologies	inner hair cells	E_02_0015	DNA-seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.		Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Immunohistochemical staining	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.			DNA-seq				Dlx5
29301908	chr6	6038754	6040754	Slc25a13	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	mouse	Inner ear	High+Lowthroughput	Deletion of a Long-Range Dlx5 Enhancer Disrupts Inner Ear Development in Mice	否		inner ear dysmorphologies	inner hair cells	E_02_0015	DNA-seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.		Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Immunohistochemical staining	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.			DNA-seq				Slc25a13
29300379	chr15	67061032	67063032	SMAD3	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	human	Thyroid	High+Lowthroughput	The role of SMAD3 in the genetic predisposition to papillary thyroid carcinoma	是	rs17293632,rs4562997	papillary thyroid carcinoma	thyroid cancer cell lines	E_01_0022	ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	Immunohistochemical staining	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	SMAD3		ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.			
29300379	chr5	142307853	142309853	SPRY4	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene	human	Thyroid	High+Lowthroughput	The role of SMAD3 in the genetic predisposition to papillary thyroid carcinoma	是	rs17293632,rs4562997	papillary thyroid carcinoma	thyroid cancer cell lines	E_01_0022	ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene		The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene	Immunohistochemical staining	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene			ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR				SPRY4
29300302	chrX	129537551	129539551	OCRL	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain	human	Kidney	High+Lowthroughput	Splicing Analysis of Exonic OCRL Mutations Causing Lowe Syndrome or Dent-2 Disease	否		Lowe syndrome and Dent-2 disease	COS7 cells	E_01_0023	Transfection,RT-PCR	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain		The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain	Immunohistochemical staining	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain			Transfection,RT-PCR				OCRL
29297498	chr16	29880412	29882412	Hes1	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.	mouse	Small intestine	High+Lowthroughput	Epithelial Hes1 maintains gut homeostasis by preventing microbial dysbiosis	否		intestinal microbial dysbiosis and disturbed homeostasis	enterocyte	E_02_0016	qPCR,Western blot	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.		Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.	Immunohistochemical staining	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.			qPCR,Western blot				Hes1
29294297	chr7	148804388	148806388	EZH2	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	human	Dental pulp tissue	High+Lowthroughput	EZH2 Impairs Human Dental Pulp Cell Mineralization via the Wnt/β-Catenin Pathway	否		Oral Diseases	dental pulp cell	E_01_0024	ChIP	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	Immunohistochemical staining	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	EZH2		ChIP	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.			
29294065	chr19	33297489	33299489	CEBPA	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	human	Adrenal tissues	High+Lowthroughput	Purkinje Cell Protein 4 Expression Is Associated With DNA Methylation Status in Aldosterone-Producing Adenoma	否		adrenocortical adenoma	cortical cell of adrenal gland	E_01_0025	qPCR,ChIP	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	Immunohistochemical staining	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	CEBPA		qPCR,ChIP	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.			
29286144	chr7	148804229	148806229	EZH2	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	human	Melanoma tissue	High+Lowthroughput	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma	否		Melanoma	melanoma cells	E_01_0026	Western blot,ChIP	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	Immunohistochemical staining	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	EZH2		Western blot,ChIP	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.			
29286132	chr7	148804179	148806179	EZH2	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	human	Kidney	High+Lowthroughput	EZH2 enhances the invasive capability of renal cell carcinoma cells via activation of STAT3	否		renal cell carcinoma	nephrocyte	E_01_0027	Western blot	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	Immunohistochemical staining	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	EZH2		Western blot	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC			
29259014	chr7	55016411	55018411	EGFR	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	human	Lung	High+Lowthroughput	"ER Stress Signaling Promotes the Survival of Cancer ""Persister Cells"" Tolerant to EGFR Tyrosine Kinase Inhibitors"	否		Tumor	PC9 cells	E_01_0028	qRT-PCR,RNA-seq	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	Immunohistochemical staining	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	EGFR		qRT-PCR,RNA-seq	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.			
29257325	chr5	88714072	88716072	MEF2C	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)	human,mouse	Heart tissue	High+Lowthroughput	Optimization and enrichment of induced cardiomyocytes derived from mouse fibroblasts by reprogramming with cardiac transcription factors	否		Ischemic heart disease	cardiac muscle cell (sensu Arthopoda)	E_02_0017	RT-qPCR,qPCR,Immunostaining	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)		The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)	Immunohistochemical staining	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)			RT-qPCR,qPCR,Immunostaining				MEF2C
29256825	chr4	108045000	108047000	LEF1	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	human	Liver	High+Lowthroughput	Salvianolic Acid B Enhances Hepatic Differentiation of Human Embryonic Stem Cells Through Upregulation of WNT Pathway and Inhibition of Notch Pathway	否		Liver disease	Hepatocytes	E_01_0029	qRT-PCR,Immunofluorescence staining,PCR,Western blot	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	Immunohistochemical staining	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	LEF1		qRT-PCR,Immunofluorescence staining,PCR,Western blot	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells			
29256171	chr10	24357349	24375452	CCN2	CCN2 is a critical matricellular protein that is expressed in several cells with major implications in physiology and different pathologies.	mouse	Connective tissue	Low+High throughput	Multiple enhancer regions govern the transcription of CCN2 during embryonic development	否	--	--	endothelial cell	E_02_0018	Transgenic mice,ChIP-seq,DNase I Hypersensitivity Assay	Four functional enhancers were identified, with each driving distinct, tissue-specific patterns of transgene expression. An enhancer located -100 kb from the CCN2 transcription start site facilitated expression within vascular tissue. An enhancer -135 kb upstream of CCN2 drove expression within the articular chondrocytes of synovial joints.The other two enhancers, located at -198 kb and -229 kb, mediated transgene expression within dermal fibroblasts, however the most prevalent activity was found within hypertrophic chondrocytes and periosteal tissue, respectively. 	Enhancer	--	PCR,Transgenic mice	Four functional enhancers were identified, with each driving distinct, tissue-specific patterns of transgene expression. An enhancer located -100 kb from the CCN2 transcription start site facilitated expression within vascular tissue. An enhancer -135 kb upstream of CCN2 drove expression within the articular chondrocytes of synovial joints.The other two enhancers, located at -198 kb and -229 kb, mediated transgene expression within dermal fibroblasts, however the most prevalent activity was found within hypertrophic chondrocytes and periosteal tissue, respectively. 	Ctgf,Fisp12,Hcs24,fisp-12	--	--	--	--	--	--	--	--	--	Ccn2
29255029	chr5	28659278	28661278	Shh	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.	mouse	Toe	High+Lowthroughput	Enhancer adoption caused by genomic insertion elicits interdigital Shh expression and syndactyly in mouse	否		syndactyly	interdigital cell	E_02_0019	ATAC-seq,PCR	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.		Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.	Immunohistochemical staining	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.			ATAC-seq,PCR				Shh
29249800	chr18	27930050	27932050	CDH2	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	human	CRPC tissues	High+Lowthroughput	DBC1 promotes castration-resistant prostate cancer by positively regulating DNA binding and stability of AR-V7	否		castration-resistant prostate cancer	castration-resistant prostate cancer cell	E_01_0030	qRT-PCR,ChIP,3C	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	Immunohistochemical staining	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	CDH2		qRT-PCR,ChIP,3C	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.			
29248547	chr7	148804663	148806663	EZH2	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	human	PCALCL tissue	High+Lowthroughput	Dual Role of EZH2 in Cutaneous Anaplastic Large Cell Lymphoma: Promoting Tumor Cell Survival and Regulating Tumor Microenvironment	否		cutaneous CD30+ lymphoproliferative disease	Primary cutaneous anaplastic T cell lymphoma cell	E_01_0031	ChIP,qRT-PCR,Western blot	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	Immunohistochemical staining	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	EZH2		ChIP,qRT-PCR,Western blot	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.			
29245050	chr13	83649881	83651881	Mef2c	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes	human,mouse	Skeletal muscle	High+Lowthroughput	NANOG restores the impaired myogenic differentiation potential of skeletal myoblasts after multiple population doublings	否		impaired myogenic differentiation potential	skeletal muscle myoblast	E_02_0020	Western blot,Immunohistochemical Staining,qPCR	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes		Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes	Immunohistochemical staining	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes			Western blot,Immunohistochemical Staining,qPCR				Mef2c
29244146	chr7	148804295	148806295	EZH2	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.	human,mouse	Embryonic tissues	High+Lowthroughput	Ezh2 Mutations Found in the Weaver Overgrowth Syndrome Cause a Partial Loss of H3K27 Histone Methyltransferase Activity	否		Weaver syndrome	chondroblast	E_02_0021	Transfection,Immunostaining	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.		It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.	Immunohistochemical staining	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.			Transfection,Immunostaining				EZH2
29233846	chr6	47504530	47506530	Ezh2	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.	human	Ovarian tissue	High+Lowthroughput	VE-Cadherin-Mediated Epigenetic Regulation of Endothelial Gene Expression	否		Ovarian carcinoma	endothelial cell	E_01_0032	Immunofluorescence,Western blot,RNA-seq ,qRT–PCR,ChIP	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.		Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.	Immunohistochemical staining	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.			Immunofluorescence,Western blot,RNA-seq ,qRT–PCR,ChIP				Ezh2
29231261	chr7	148804801	148806801	EZH2	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	human	Bladder tissue	High+Lowthroughput	LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression	否		bladder cancer	human bladder epithelial cell line	E_01_0033	Transfection,qRT-PCR,Western blot,ChIP	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	Immunohistochemical staining	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	EZH2		Transfection,qRT-PCR,Western blot,ChIP	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.			
29227829	chr6	135178878	135180878	MYB	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	human	Hematopoietic tissue	High+Lowthroughput	A long noncoding RNA from the HBS1L-MYB intergenic region on chr6q23 regulates human fetal hemoglobin expression	是	rs66650371	sickle cell disease and β-thalassemia	HUDEP-2 cell	E_01_0034	RT–PCR,qPCR,Western blot	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.		HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Immunohistochemical staining	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.			RT–PCR,qPCR,Western blot				MYB
29227829	chr6	134957756	134959756	HBS1L	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	human	Hematopoietic tissue	High+Lowthroughput	A long noncoding RNA from the HBS1L-MYB intergenic region on chr6q23 regulates human fetal hemoglobin expression	否		sickle cell disease and β-thalassemia	HUDEP-2 cell	E_01_0034	RT–PCR,qPCR,Western blot	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.		HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Immunohistochemical staining	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.			RT–PCR,qPCR,Western blot				HBS1L
29223978	chr7	148804763	148806763	EZH2	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.	mouse	Cartilage	High+Lowthroughput	PRC2 Is Dispensable in Vivo for β-Catenin-Mediated Repression of Chondrogenesis in the Mouse Embryonic Cranial Mesenchyme	否			chondroblast	E_02_0022	Immunofluorescencet,RNA-seq ,RT–qPCR,ChIP-seq	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.		Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.	Immunohistochemical staining	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.			Immunofluorescencet,RNA-seq ,RT–qPCR,ChIP-seq				EZH2
29220426	chr13	116431913	116433913	Isl1	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).	mouse	Liver	High+Lowthroughput	Isl1β Overexpression With Key β Cell Transcription Factors Enhances Glucose-Responsive Hepatic Insulin Production and Secretion	否		diabete	b cell	E_02_0023	Western blot,Luciferase Reporter Assay,qRT-PCR	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).		Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).	Immunohistochemical staining	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).			Western blot,Luciferase Reporter Assay,qRT-PCR				Isl1
29207119	chr7	148804312	148806312	EZH2	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	human	Breast	High+Lowthroughput	EZH2 inhibition sensitizes tamoxifen?resistant breast cancer cells through cell cycle regulation	否		breast cancer	breast cancer cell	E_01_0035	Transfection,RT-qPCR,Western blot	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	Immunohistochemical staining	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	EZH2		Transfection,RT-qPCR,Western blot	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.			
29207028	chr5	88714236	88716236	MEF2C	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.	human,mouse	Muscle	High+Lowthroughput	Role of the cofilin 2 gene in regulating the myosin heavy chain genes in mouse myoblast C2C12 cells	否		myofibrillar formation.	C2C12 cells	E_02_0024	RT-qPCR,RT-PCR,Western blot	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.		Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.	Immunohistochemical staining	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.			RT-qPCR,RT-PCR,Western blot				MEF2C
29203251	chrX	67541434	67543434	AR	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)	human,mouse	Prostate	High+Lowthroughput	Androgen receptor (AR) degradation enhancer ASC-J9(?) in an FDA-approved formulated solution suppresses castration resistant prostate cancer cell growth	否		prostate cancer	prostate cancer cell	E_02_0025	Western blot,qPCR	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)		Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)	Immunohistochemical staining	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)			Western blot,qPCR				AR
29180489	chr12	114350941	114352941	TBX5	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	human	Lymphoid tissue	High+Lowthroughput	Downregulation of NFAT3 Due to Lack of T-Box Transcription Factor TBX5 Is Crucial for Cytokine Expression in T Cells	否			T cell	E_01_0036	Transfection	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	Immunohistochemical staining	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	TBX5		Transfection	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.			
29180467	chr11	102107486	102109486	YAP1	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.	human,mouse	Bladder tissue	High+Lowthroughput	YAP1 and COX2 Coordinately Regulate Urothelial Cancer Stem-like Cells	否		urothelial carcinoma	urothelial cell	E_02_0026	Western blot,PCR	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.		In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.	Immunohistochemical staining	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.			Western blot,PCR				YAP1
29180467	chr3	181708705	181710705	SOX2	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.	human,mouse	Bladder tissue	High+Lowthroughput	YAP1 and COX2 Coordinately Regulate Urothelial Cancer Stem-like Cells	否		urothelial carcinoma	urothelial cell	E_02_0026	Western blot,PCR	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.		Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.	Immunohistochemical staining	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.			Western blot,PCR				SOX2
29180399	chr19	15232268	15234268	BRD4	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.	human,mouse	Skin tissue	High+Lowthroughput	Diminished microRNA-29b level is associated with BRD4-mediated activation of oncogenes in cutaneous T-cell lymphoma	否		cutaneous T-cell lymphoma	T cell	E_02_0027	RT-PCR,ChIP,Transfection	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.		We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.	Immunohistochemical staining	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.			RT-PCR,ChIP,Transfection				BRD4
29177481	chr7	148804952	148806952	EZH2	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	human		High+Lowthroughput	CDYL1 fosters double-strand break-induced transcription silencing and promotes homology-directed repair	否				E_01_0037	Transfection,Immunofluorescence,Western blot,ChIP	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	Immunohistochemical staining	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	EZH2		Transfection,Immunofluorescence,Western blot,ChIP	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.			
29175454	chr10	68557509	68559509	TET1	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	human	Tumor	High+Lowthroughput	Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells	否		iAs-mediated carcinogenesis	transformed cell	E_01_0038	qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Immunohistochemical staining	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	TET1		qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.			
29175454	chr4	105143899	105145899	TET2	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	human	Tumor	High+Lowthroughput	Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells	否		iAs-mediated carcinogenesis	transformed cell	E_01_0038	qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.		To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Immunohistochemical staining	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.			qRT-PCR,ChIP				TET2
29175454	chr16	67559779	67561779	CTCF	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	human	Tumor	High+Lowthroughput	Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells	否		iAs-mediated carcinogenesis	transformed cell	E_01_0038	qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Immunohistochemical staining	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	CTCF		qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.			
29162563	chr16	86507790	86509790	FOXF1	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	human	Gastrointestinal tract	High+Lowthroughput	FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor	否		gastrointestinal stromal tumor	gastrointestinal stromal tumor cell	E_01_0039	siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	Immunohistochemical staining	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	FOXF1		siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.			
29162563	chr7	13888509	13890509	ETV1	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	human	Gastrointestinal tract	High+Lowthroughput	FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor	否		gastrointestinal stromal tumor	gastrointestinal stromal tumor cell	E_01_0039	siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Immunohistochemical staining	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	ETV1		siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis			
29162563	chr4	54654533	54656533	KIT	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	human	Gastrointestinal tract	High+Lowthroughput	FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor	否		gastrointestinal stromal tumor	gastrointestinal stromal tumor cell	E_01_0039	siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Immunohistochemical staining	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	KIT		siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis			
29162511	chr1	11782707	11784707	MTHFR	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs1801133	thymic lymphoid hyperplasia	B cell	E_01_0040		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Immunohistochemical staining	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis							MTHFR
29162511	chr1	236792078	236794078	MTR	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs1805087	thymic lymphoid hyperplasia	B cell	E_01_0040		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Immunohistochemical staining	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis							MTR
29162511	chr18	654552	656552	TYMS	Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs45445694	thymic lymphoid hyperplasia	B cell	E_01_0040		Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients		Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients	Immunohistochemical staining	Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients							TYMS
29162511	chr5	7849068	7851068	MTRR	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs1801394	thymic lymphoid hyperplasia	B cell	E_01_0040		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Immunohistochemical staining	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis							MTRR
29158184	chr11	112670256	112672256	Sox9	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis	mouse	Kidney	High+Lowthroughput	TGF-β-mediated upregulation of Sox9 in fibroblast promotes renal fibrosis	否		renal fibrosis	kidney fibroblast cell	E_02_0028	Transfection,qPCR,ChIP	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis		These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis	Immunohistochemical staining	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis			Transfection,qPCR,ChIP				Sox9
29155305	chr3	8725613	8727613	Hey1	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	mouse	Tooth germ	High+Lowthroughput	Hey1 and Hey2 are differently expressed during mouse tooth development	否		tooth injury	dental mesenchymal cell	E_02_0029	qRT-PCR	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development		Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Immunohistochemical staining	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development			qRT-PCR				Hey1
29155305	chr10	30705725	30707725	Hey2	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	mouse	Tooth germ	High+Lowthroughput	Hey1 and Hey2 are differently expressed during mouse tooth development	否		tooth injury	dental mesenchymal cell	E_02_0029	qRT-PCR	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development		Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Immunohistochemical staining	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development			qRT-PCR				Hey2
29154949	chr12	56115695	56117695	ESYT1	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	human	Lung CF tissue	High+Lowthroughput	A novel microscopy-based assay identifies extended synaptotagmin-1 (ESYT1) as a positive regulator of anoctamin 1 traffic	否		Cystic Fibrosis	bronchial epithelial cell	E_01_0041	siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.		We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Immunohistochemical staining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.			siRNA transfection,Immunostaining				ESYT1
29154949	chr11	69983331	69985331	ANO1	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	human	Lung CF tissue	High+Lowthroughput	A novel microscopy-based assay identifies extended synaptotagmin-1 (ESYT1) as a positive regulator of anoctamin 1 traffic	否		Cystic Fibrosis	bronchial epithelial cell	E_01_0041	siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Immunohistochemical staining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	ANO1		siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.			
29154949	chr11	14440611	14442611	COPB1	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	human	Lung CF tissue	High+Lowthroughput	A novel microscopy-based assay identifies extended synaptotagmin-1 (ESYT1) as a positive regulator of anoctamin 1 traffic	否		Cystic Fibrosis	bronchial epithelial cell	E_01_0041	siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.		We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Immunohistochemical staining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.			siRNA transfection,Immunostaining				COPB1
29154784	chr16	29880401	29882401	Hes1	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures	mouse	Liver	High+Lowthroughput	TGF-β1 signaling regulates mouse hepatic stellate cell differentiation via the Jagged1/Notch pathway	否		liver disease	hepatic stellate cell	E_02_0030	Western blot,ChIP,Transfection,qRT-PCR,Immunofluorescence	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures		Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures	Immunohistochemical staining	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures			Western blot,ChIP,Transfection,qRT-PCR,Immunofluorescence				Hes1
29148101	chr3	130901584	130903584	Lef1	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.	mouse	Tooth-germ	High+Lowthroughput	Homeobox protein MSX-1 inhibits expression of bone morphogenetic protein 2, bone morphogenetic protein 4, and lymphoid enhancer-binding factor 1 via Wnt/β-catenin signaling to prevent differentiation of dental mesenchymal cells during the late bell stage	否		congenital tooth agenesis	dental mesenchymal cell	E_02_0031	Western blot,qPCR	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.		Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.	Immunohistochemical staining	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.			Western blot,qPCR				Lef1
29142074	chr7	94002773	94005073	STAT3	Yet, a certain threshold level of STAT3 activity is essential to support activation of the COL1A2 enhancer and TGFβ signalling in fibroblasts.	human	Lung	Low throughput	STAT3 controls COL1A2 enhancer activation cooperatively with JunB, regulates type I collagen synthesis posttranscriptionally, and is essential for lung myofibroblast differentiation	否	--	--	Myofibroblast	E_02_0032	Luciferase Reporter Assay,ChIP	The structure of the COL1A2 far-upstream enhancer and the HS4 region is shown in Figure 1A.Enhancer activation was determined by measuring luciferase expression.	Enhancer	--	Luciferase Reporter Assay,ChIP	We created two different luciferase reporter gene constructs under the control of the COL1A2 enhancer and proximal promoter.When the enhancer is engaged, it contacts the RNA polymerase complex forming at the collagen promoter. Thus, an RNA polymerase ChIP signal is a direct measure of enhancer engagement. 	EDSARTH2,EDSCV,OI4	--	--	--	STAT3	ADMIO,ADMIO1,APRF,HIES	ChIP-qPCR	ChIP analysis using qPCR for the binding of STAT3, JunB, and RNA polymerase II, in the HS4 region of SSc fibroblasts after treatment with SD1029, STAT3 siRNA (siSTAT3), or nontargeting siRNA (siNT). * = p < 0.05.	--	--	COL1A2
29142074	chr7	94002773	94005073	COL1A2	Yet, a certain threshold level of STAT3 activity is essential to support activation of the COL1A2 enhancer and TGFβ signalling in fibroblasts.	human	Lung	Low throughput	STAT3 controls COL1A2 enhancer activation cooperatively with JunB, regulates type I collagen synthesis posttranscriptionally, and is essential for lung myofibroblast differentiation	否	--	--	Myofibroblast	E_02_0032	Luciferase Reporter Assay,ChIP	The structure of the COL1A2 far-upstream enhancer and the HS4 region is shown in Figure 1A.Enhancer activation was determined by measuring luciferase expression.	Enhancer	--	Luciferase Reporter Assay,ChIP	We created two different luciferase reporter gene constructs under the control of the COL1A2 enhancer and proximal promoter.When the enhancer is engaged, it contacts the RNA polymerase complex forming at the collagen promoter. Thus, an RNA polymerase ChIP signal is a direct measure of enhancer engagement. 	EDSARTH2,EDSCV,OI4	--	--	--	STAT3	ADMIO,ADMIO1,APRF,HIES	ChIP-qPCR	ChIP analysis using qPCR for the binding of STAT3, JunB, and RNA polymerase II, in the HS4 region of SSc fibroblasts after treatment with SD1029, STAT3 siRNA (siSTAT3), or nontargeting siRNA (siNT). * = p < 0.05.	--	--	COL1A2
29141987	chr2	103887795	103888195	Lmo2	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	mouse	Embryo	Low+High throughput	BRACHYURY directs histone acetylation to target loci during mesoderm development	否	--	--	hematopoietic and endothelial cell	E_02_0033	ChIP-seq	We overlapped TBS with genome‐wide H3K4me1 peaks from T WT mesodermal cells and found the same trend of decreased H3K27ac within ±1 kb of TBS/H3K4me1 sites (Fig EV4E), suggesting that T functions to coordinate H3K27ac at putative enhancer regions throughout the genome, and may regulate the switch between poised H3K4me1(+) enhancers and active H3K27ac/H3K4me1(+) enhancer regions.	Enhancer	--	RT-qPCR,ChIP-qPCR,ChIP-seq	Both the ?70 enhancer and the TSS of Lmo2 display a decrease in H3K27ac in T Y88A mutant mesodermal cells, in the ChIP‐Seq data and confirmed by ChIP‐qPCR (Figs ?(Figs5A5A and B, and EV5A). We reasoned that T binding to the ?70 enhancer of Lmo2 may recruit permissive chromatin marks to the TSS to regulate expression, and that this regulation is disrupted in T Y88A mutant mesodermal cells.	Rbtn-2,Rbtn2,Rhom-2,Ttg2	--	--	--	T	Bra,D17Mit170,Low,Lr1,Tbxt,Tl2,Tl3,cou,me75,T	ChIP-seq,ChIP-qPCR	We performed a co-immunoprecipitation analysis from in vitrodifferentiated mesodermal cells and found an interaction between endogenous T and p300.Strikingly, loss of H3K27ac was found at TBS upstream of the T genomic locus itself by ChIP-Seq . We validated this decrease in H3K27ac at the T genomic locus by ChIP-qPCR in TY88A and TWT mesodermal cells differentiated in vitro.	--	--	Lmo2
29141987	chr2	103887795	103888195	T	Here, we show that cooperative function of BRACHYURY (T) with histone-modifying enzymes is essential for mouse embryogenesis.	mouse	Embryo	Low+High throughput	BRACHYURY directs histone acetylation to target loci during mesoderm development	否	--	--	hematopoietic and endothelial cell	E_02_0033	ChIP-seq	We overlapped TBS with genome‐wide H3K4me1 peaks from T WT mesodermal cells and found the same trend of decreased H3K27ac within ±1 kb of TBS/H3K4me1 sites (Fig EV4E), suggesting that T functions to coordinate H3K27ac at putative enhancer regions throughout the genome, and may regulate the switch between poised H3K4me1(+) enhancers and active H3K27ac/H3K4me1(+) enhancer regions.	Enhancer	--	RT-qPCR,ChIP-qPCR,ChIP-seq	Both the ?70 enhancer and the TSS of Lmo2 display a decrease in H3K27ac in T Y88A mutant mesodermal cells, in the ChIP‐Seq data and confirmed by ChIP‐qPCR (Figs ?(Figs5A5A and B, and EV5A). We reasoned that T binding to the ?70 enhancer of Lmo2 may recruit permissive chromatin marks to the TSS to regulate expression, and that this regulation is disrupted in T Y88A mutant mesodermal cells.	Rbtn-2,Rbtn2,Rhom-2,Ttg2	--	--	--	T	Bra,D17Mit170,Low,Lr1,Tbxt,Tl2,Tl3,cou,me75,T	ChIP-seq,ChIP-qPCR	We performed a co-immunoprecipitation analysis from in vitrodifferentiated mesodermal cells and found an interaction between endogenous T and p300.Strikingly, loss of H3K27ac was found at TBS upstream of the T genomic locus itself by ChIP-Seq . We validated this decrease in H3K27ac at the T genomic locus by ChIP-qPCR in TY88A and TWT mesodermal cells differentiated in vitro.	--	--	Lmo2
29138985	chr4	108044731	108046731	LEF1	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells	human,mouse	Skin tissue	High+Lowthroughput	Effects of microRNA-708 on Epithelial-Mesenchymal Transition, Cell Proliferation and Apoptosis in Melanoma Cells by Targeting LEF1 through the Wnt Signaling Pathway	否		Melanoma	Melanoma Cell Line	E_02_0034	RT-qPCR,Dual-Luciferase Reporter Assay	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells		Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells	Immunohistochemical staining	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells			RT-qPCR,Dual-Luciferase Reporter Assay				LEF1
29138798	chr3	8725482	8727482	Hey1	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.	mouse	Dental pulp tissue	High+Lowthroughput	Hey1 functions as a positive regulator of odontogenic differentiation in odontoblast?lineage cells	否		Oral Disease	odontoblast	E_02_0035	Western blot,ChIP,Transfection,RT‑qPCR,Immunofluorescence staining	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.		Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.	Immunohistochemical staining	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.			Western blot,ChIP,Transfection,RT‑qPCR,Immunofluorescence staining				Hey1
29129693	chr17	76133482	76135482	FOXJ1	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	human	Bladder cancer tissues	High+Lowthroughput	FOXJ1 promotes bladder cancer cell growth and regulates Warburg effect	否		bladder cancer	bladder cancer cell	E_01_0042	Western blot	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	Immunohistochemical staining	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	FOXJ1		Western blot	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.			
29127222	chr15	99562705	99564705	MEF2A	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	MEF2A		Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			
29127222	chr19	19143005	19145005	MEF2B	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.		These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR				MEF2B
29127222	chr5	88714205	88716205	MEF2C	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	MEF2C		Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			
29127222	chr1	156460887	156462887	MEF2D	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.		These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR				MEF2D
29113912	chr14	18175266	18186392	Ang2	Importantly, sorafenib treatment, which suppresses H3K27 acetylation and Ang2 expression, profoundly halts the progression of Arid1a-deficient HCCs	mouse	Liver	Low+High throughput	Arid1a regulates response to anti-angiogenic therapy in advanced hepatocellular carcinoma	否	--	Hepatocellular Carcinoma	HCC cell lines	E_02_0036	ChIP-seq	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Enhancer	--	ChIP-seq,ChIP-qPCR	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Angrp,Raa3,Rnase5b	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq,ChIP-PCR	Interestingly,published ChIP-seq data also showed that p300 bound to the Ang2 gene locus, as we validated by ChIP-PCR.	--	--	Ang2
29113912	chr14	18175266	18186392	Arid1a	Arid1a-deficiency promotes Ang2- dependent angiogenesis leading to hepatocellular carcinoma progression.	mouse	Liver	Low+High throughput	Arid1a regulates response to anti-angiogenic therapy in advanced hepatocellular carcinoma	否	--	Hepatocellular Carcinoma	HCC cell lines	E_02_0036	ChIP-seq	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Enhancer	--	ChIP-seq,ChIP-qPCR	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Angrp,Raa3,Rnase5b	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq,ChIP-PCR	Interestingly,published ChIP-seq data also showed that p300 bound to the Ang2 gene locus, as we validated by ChIP-PCR.	--	--	Ang2
29107694	chr7	148804477	148806477	EZH2	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription	human,mouse	Pancreas	High+Lowthroughput	Chaetospirolactone reverses the apoptotic resistance towards TRAIL in pancreatic cancer	否		pancreatic cancer	pancreatic cancer cell	E_02_0037	Western blot,ChIP,qPCR	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription		Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription	Immunohistochemical staining	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription			Western blot,ChIP,qPCR				EZH2
29106960	chr7	148804589	148806589	EZH2	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	human	Liver	High+Lowthroughput	Carnosol-mediated Sirtuin 1 activation inhibits Enhancer of Zeste Homolog 2 to attenuate liver fibrosis	否		hepatic fibrosis	Myofibroblast	E_01_0044	Western blot, RT-PCR,Immunofluorescence staining,Transfection	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	Immunohistochemical staining	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	EZH2		Western blot, RT-PCR,Immunofluorescence staining,Transfection	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.			
29089464	chr7	148804445	148806445	EZH2	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	human	Breast cancer tissue	High+Lowthroughput	Correlations of EZH2 and SMYD3 gene polymorphisms with breast cancer susceptibility and prognosis	否		breast cancer	breast cancer cell	E_01_0045	RT-qPCR,Western blot	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	Immunohistochemical staining	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	EZH2		RT-qPCR,Western blot	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation			
29070695	chr17	19492823	19494823	SLC47A1	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.	human	Liver	High+Lowthroughput	Relationship between DNA Methylation in the 5' CpG Island of the SLC47A1 (Multidrug and Toxin Extrusion Protein MATE1) Gene and Interindividual Variability in MATE1 Expression in the Human Liver	否			HepG2 cell	E_01_0046	qRT-PCR	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.		These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.	Immunohistochemical staining	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.			qRT-PCR				SLC47A1
29059175	chr16	67559364	67561364	CTCF	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	human	Tumor	High+Lowthroughput	Induction of anti-VEGF therapy resistance by upregulated expression of microseminoprotein (MSMP)	否		Tumor	cancer cell	E_01_0047	qRT–PCR,Immunostaining,Western blot	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	Immunohistochemical staining	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	CTCF		qRT–PCR,Immunostaining,Western blot	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.			
29059175	chr9	35749798	35751798	MSMP	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy	human	Tumor	High+Lowthroughput	Induction of anti-VEGF therapy resistance by upregulated expression of microseminoprotein (MSMP)	否		Tumor	cancer cell	E_01_0047	qRT–PCR,Immunostaining,Western blot	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy		These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy	Immunohistochemical staining	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy			qRT–PCR,Immunostaining,Western blot				MSMP
29059150	chr12	54572339	54574339	PPP1R1A	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element	human,mouse	Tumor	High+Lowthroughput	Protein phosphatase 1 regulatory subunit 1A in ewing sarcoma tumorigenesis and metastasis	否		ewing sarcoma	ewing sarcoma cell	E_02_0038	qRT–PCR,ChIP-Seq,Luciferase reporter assay	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element		We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element	Immunohistochemical staining	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element			qRT–PCR,ChIP-Seq,Luciferase reporter assay				PPP1R1A
29054992	chr5	69231968	69233968	CDK7	CDK7 is a key regulator of the cell cycle	mouse	Tumor	High+Lowthroughput	Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression	否		Tumor	cancer cell	E_02_0039	RNA-seq,ChIP-Seq,ChIP,RT-PCR	CDK7 is a key regulator of the cell cycle	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CDK7 is a key regulator of the cell cycle		CDK7 is a key regulator of the cell cycle	Immunohistochemical staining	CDK7 is a key regulator of the cell cycle			RNA-seq,ChIP-Seq,ChIP,RT-PCR				CDK7
29053336	chr7	148804334	148806334	EZH2	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	human	Lung	High+Lowthroughput	Interplay between EZH2 and G9a Regulates CXCL10 Gene Repression in Idiopathic Pulmonary Fibrosis	否		Pulmonary Fibrosis		E_01_0048	ChIP	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	Immunohistochemical staining	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	EZH2		ChIP	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.			
29044515	chr12	32787839	32789839	PKP2	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.	human	Colon tissue	High+Lowthroughput	The human PKP2/plakophilin-2 gene is induced by Wnt/β-catenin in normal and colon cancer-associated fibroblasts	否		colon cancer	colon cancer-associated fibroblast	E_01_0049	RNA-Seq,RT-qPCR,Western blot	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.		Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.	Immunohistochemical staining	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.			RNA-Seq,RT-qPCR,Western blot				PKP2
29024000	chr16	29880620	29882620	Hes1	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.	mouse	Liver	High+Lowthroughput	Myeloid Notch1 deficiency activates the RhoA/ROCK pathway and aggravates hepatocellular damage in mouse ischemic livers	否		Liver Injury	hepatocyte	E_02_0040	Immunohistochemistry staining,qRT-PCR,Immunofluorescence staining	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.		In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.	Immunohistochemical staining	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.			Immunohistochemistry staining,qRT-PCR,Immunofluorescence staining				Hes1
28994199	chr1	47213269	47215269	TAL1	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	human	Haematopoietic tissue	High+Lowthroughput	Inhibition of MEK/ERK signalling pathway promotes erythroid differentiation and reduces HSCs engraftment in ex?vivo expanded haematopoietic stem cells	否			hematopoietic stem cell	E_01_0050	qPCR,Immunohistochemical staining	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	Immunohistochemical staining	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	TAL1		qPCR,Immunohistochemical staining	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation			
28974397	chr7	148804688	148806688	EZH2	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	human	Soft tissue	High+Lowthroughput	Comprehensive Genomic Sequencing of Urothelial Tumors Identifies Rare SMARCB1 (INI-1)-Deficient Carcinomas of the Urinary?System	否		urothelial carcinoma	tumor cell	E_01_0051	Immunohistochemical staining	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	Immunohistochemical staining	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	EZH2		Immunohistochemical staining	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.			
28974397	chr22	23784056	23786056	SMARCB1	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.	human	Soft tissue	High+Lowthroughput	Comprehensive Genomic Sequencing of Urothelial Tumors Identifies Rare SMARCB1 (INI-1)-Deficient Carcinomas of the Urinary?System	否		urothelial carcinoma	tumor cell	E_01_0051	Immunohistochemical staining	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.		Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.	Immunohistochemical staining	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.			Immunohistochemical staining				SMARCB1
28971975	chr17	61449600	61451600	TBX4	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	human		High+Lowthroughput	TBX4 is involved in the super-enhancer-driven transcriptional programs underlying features specific to lung fibroblasts	否		pathogenesis of respiratory diseases	lung fibroblasts cell	E_01_0052	RNA-seq,RT-PCR	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	Immunohistochemical staining	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	TBX4		RNA-seq,RT-PCR	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.			
28970250	chr7	148804484	148806484	EZH2	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.	human,mouse	Liver	High+Lowthroughput	SIRT1 antagonizes liver fibrosis by blocking hepatic stellate cell activation in mice	否		liver fibrosis	hepatic stellate cell	E_02_0041	Western blot, qPCR,Transfection,ChIP	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.		Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.	Immunohistochemical staining	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.			Western blot, qPCR,Transfection,ChIP				EZH2
28951561	chr17	42697786	42699786	EZH1	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	human,mouse	Bone marrow	High+Lowthroughput	Dual inhibition of EZH1/2 breaks the quiescence of leukemia stem cells in acute myeloid leukemia	否		Acute myeloid leukemia	leukemia stem cell	E_02_0042	Western blot	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.		Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Immunohistochemical staining	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.			Western blot				EZH1
28951561	chr7	148804920	148806920	EZH2	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	human,mouse	Bone marrow	High+Lowthroughput	Dual inhibition of EZH1/2 breaks the quiescence of leukemia stem cells in acute myeloid leukemia	否		Acute myeloid leukemia	leukemia stem cell	E_02_0042	Western blot	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.		Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Immunohistochemical staining	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.			Western blot				EZH2
28939663	chr7	148804966	148806966	EZH2	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	human	Liver	High+Lowthroughput	Hepatoma-intrinsic CCRK inhibition diminishes myeloid-derived suppressor cell immunosuppression and enhances immune-checkpoint blockade efficacy	否		hepatocellular carcinoma	Myeloid-derived suppressor cell	E_01_0053	Transfection	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	Immunohistochemical staining	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	EZH2		Transfection	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets			
28925507	chr7	148804490	148806490	EZH2	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	human	CRC tissue	High+Lowthroughput	(-)-Epigallocatechin-3-gallate and EZH2 inhibitor GSK343 have similar inhibitory effects and mechanisms of action on colorectal cancer cells	否		colorectal cancer	colorectal cancer (CRC) cell line	E_01_0054	Western blot,Immunofluorescence	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	Immunohistochemical staining	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	EZH2		Western blot,Immunofluorescence	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.			
28925391	chr7	148804797	148806797	EZH2	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	human	Tumor	High+Lowthroughput	EZH2 contributes to the response to PARP inhibitors through its PARP-mediated poly-ADP ribosylation in breast cancer	否		breast cancer	breast cancer cell	E_01_0055	ChIP,qPCR,RT-qPCR,Western blot	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	Immunohistochemical staining	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	EZH2		ChIP,qPCR,RT-qPCR,Western blot	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.			
28923345	chr10	67881952	67883952	SIRT1	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	human		High+Lowthroughput	SIRT1 is a transcriptional enhancer of the glucocorticoid receptor acting independently to its deacetylase activity	否			HeLa cell	E_01_0056	Transfection,Western blot,RNA-seq,PCR,ChIP	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	Immunohistochemical staining	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	SIRT1		Transfection,Western blot,RNA-seq,PCR,ChIP	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.			
28922471	chr19	35742614	35744614	PSENEN	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.	human		High+Lowthroughput	A phenotype combining hidradenitis suppurativa with Dowling-Degos disease caused by a founder mutation in PSENEN	否		Dowling-Degos disease	keratinocyte cell	E_01_0057	qRT-PCR	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.		The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.	Immunohistochemical staining	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.			qRT-PCR				PSENEN
28902616	chr5	88714680	88716680	MEF2C	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	human	Heart	High+Lowthroughput	MEF2C loss-of-function mutation associated with familial dilated cardiomyopathy	否		dilated cardiomyopathy	HeLa cell	E_01_0058	Transfection,dual-luciferase reporter assay	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	Immunohistochemical staining	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	MEF2C		Transfection,dual-luciferase reporter assay	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).			
28898113	chr1	209782978	209784978	IRF6	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.	human,mouse	Salivary gland	High+Lowthroughput	Interferon Regulatory Factor 6 Is Necessary for Salivary Glands and Pancreas Development	否		xerostomia	acinar cell	E_02_0043	Immunofluorescent Staining,RNA-Seq	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.		Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.	Immunohistochemical staining	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.			Immunofluorescent Staining,RNA-Seq				IRF6
28862715	chr7	148804307	148806307	EZH2	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	human	Tumor	High+Lowthroughput	Prognostic role of EZH2 in gliomas: a meta-analysis	否		gliomas	tumor cell	E_01_0059	Meta-analysis	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	Immunohistochemical staining	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	EZH2		Meta-analysis	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.			
28858300	chr7	148804693	148806693	EZH2	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	human	Tumor	High+Lowthroughput	Development of a high-throughput fluorescence polarization assay for the discovery of EZH2-EED interaction inhibitors	否		Tumor	cancer cell	E_01_0060	PCR	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	Immunohistochemical staining	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	EZH2		PCR	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.			
28811072	chr16	81236	83236	NPRL3	One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.	human		High+Lowthroughput	Evolution of hemoglobin loci and their regulatory elements	否			erythroid cell	E_01_0061		One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.		One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.	Immunohistochemical staining	One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.							NPRL3
28810932	chr7	148804688	148806688	EZH2	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	human	CCA tissue	High+Lowthroughput	Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells	否		cholangiocarcinoma	Cholangiocarcinoma Cell	E_01_0062	qRT-PCR,ChIP,Western blot	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	Immunohistochemical staining	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	EZH2		qRT-PCR,ChIP,Western blot	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.			
28796375	chr7	148804611	148806611	EZH2	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	human	LA tissue	High+Lowthroughput	Effects of long noncoding RNA SPRY4-IT1-mediated EZH2 on the invasion and migration of lung adenocarcinoma	否		lung adenocarcinoma	lung adenocarcinoma (LA) cell	E_01_0063	Western blot,RT-qPCR	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	Immunohistochemical staining	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	EZH2		Western blot,RT-qPCR	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.			
28795320	chr7	148804483	148806483	EZH2	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	human	Laryngeal carcinoma tissue	High+Lowthroughput	EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma	否		laryngeal carcinoma	laryngeal carcinoma cell	E_01_0064	Western blot,qRT-PCR	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	Immunohistochemical staining	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	EZH2		Western blot,qRT-PCR	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.			
28774779	chr12	57092763	57094763	STAT6	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	human		High+Lowthroughput	Extensive and functional overlap of the STAT6 and RXR cistromes in the active enhancer repertoire of human CD14+ monocyte derived differentiating macrophages	否			macrophage	E_01_0065	ChIP,ChIP-seq,RNA-Seq,qPCR	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	Immunohistochemical staining	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	STAT6		ChIP,ChIP-seq,RNA-Seq,qPCR	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.			
28763207	chr7	148804454	148806454	EZH2		human		High+Lowthroughput	Inhibition of Human Enhancer of Zeste Homolog 2 with Tambjamine Analogs	否				E_01_0066	Immunofluorescence staining		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining		EZH2		Immunofluorescence staining				
28763207	chr9	128680837	128682837	SET		human		High+Lowthroughput	Inhibition of Human Enhancer of Zeste Homolog 2 with Tambjamine Analogs	否				E_01_0066	Immunofluorescence staining		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				Immunofluorescence staining				SET
28763207	chr12	19401102	19403102	AEBP2		human		High+Lowthroughput	Inhibition of Human Enhancer of Zeste Homolog 2 with Tambjamine Analogs	否				E_01_0066	Immunofluorescence staining		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				Immunofluorescence staining				AEBP2
28752422	chr16	15702106	15704106	Cebpd	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	mouse	Bone	High+Lowthroughput	Regulation of Clock Genes by Adrenergic Receptor Signaling in Osteoblasts	否			cementoblast	E_02_0044		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Immunohistochemical staining	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.							Cebpd
28752422	chr14	46618115	46620115	Bmp4	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	mouse	Bone	High+Lowthroughput	Regulation of Clock Genes by Adrenergic Receptor Signaling in Osteoblasts	否			cementoblast	E_02_0044		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Immunohistochemical staining	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.							Bmp4
28752422	chr13	53118269	53120269	Nfil3	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	mouse	Bone	High+Lowthroughput	Regulation of Clock Genes by Adrenergic Receptor Signaling in Osteoblasts	否			cementoblast	E_02_0044		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Immunohistochemical staining	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.							Nfil3
28744818	chr9	81580972	81582972	TLE1	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	mouse	Small intestine	High+Lowthroughput	Epigenetic modification of TLE1 induce abnormal differentiation in diabetic mice intestinal epithelium	否		diabetes mellitus	enterocyte	E_02_0045	Western Blot,RT-PCR,Dual-luciferase reporter assay	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice		Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Immunohistochemical staining	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice			Western Blot,RT-PCR,Dual-luciferase reporter assay				TLE1
28744818	chr16	29880216	29882216	Hes1	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	mouse	Small intestine	High+Lowthroughput	Epigenetic modification of TLE1 induce abnormal differentiation in diabetic mice intestinal epithelium	否		diabetes mellitus	enterocyte	E_02_0045	Western Blot,RT-PCR,Dual-luciferase reporter assay	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice		Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Immunohistochemical staining	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice			Western Blot,RT-PCR,Dual-luciferase reporter assay				Hes1
28722764	chr7	148804258	148806258	EZH2	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	human		High+Lowthroughput	12-O-tetradecanoylphorbol-13-acetate and EZH2 inhibition: A novel approach for promoting myogenic differentiation in embryonal rhabdomyosarcoma cells	否		Rhabdomyosarcoma	myocyte	E_01_0067	Western blot,Real-Time PCR	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	Immunohistochemical staining	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	EZH2		Western blot,Real-Time PCR	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.			
28720764	chr7	148804667	148806667	EZH2	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	mouse	Bone marrow	High+Lowthroughput	High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis	否		myelodysplastic syndromes	bone marrow cell	E_02_0046	SQ-RT-PCR,ChIP	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.		The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Immunohistochemical staining	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.			SQ-RT-PCR,ChIP				EZH2
28720764	chr6	58558640	58560640	Abcg2	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	mouse	Bone marrow	High+Lowthroughput	High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis	否		myelodysplastic syndromes	bone marrow cell	E_02_0046	SQ-RT-PCR,ChIP	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.		The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Immunohistochemical staining	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.			SQ-RT-PCR,ChIP				Abcg2
28718381	chr7	148804593	148806593	EZH2	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	human	Ectopic endometrial tissue	High+Lowthroughput	Histological and Immunohistochemical Characterization of the Similarity and Difference Between Ovarian Endometriomas and Deep Infiltrating Endometriosis	否		Ovarian endometrioma (OMA) and deep infiltrating endometriosis (DIE)	endothelial cell	E_01_0068	immunostaining	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	Immunohistochemical staining	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	EZH2		immunostaining	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.			
28681918	chr7	148804320	148806320	EZH2	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	human	Cervical epithelial tissue	High+Lowthroughput	MicroRNA-137 is negatively associated with clinical outcome and regulates tumor development through EZH2 in cervical cancer	否		cervical cancer	CC cell line	E_01_0069	qPCR,Dual-luciferase reporter assay	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	Immunohistochemical staining	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	EZH2		qPCR,Dual-luciferase reporter assay	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions			
28681114	chr7	148804493	148806493	EZH2	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	human	Tumor	High+Lowthroughput	Predicting the Correlation of EZH2 and Cancer Stem Cell Markers in Esophageal Squamous Cell Carcinoma	否		Esophageal Squamous Cell Carcinoma	Cancer Stem Cell	E_01_0070	qRT-PCR	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	EZH2		qRT-PCR	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.			
28621459	chr1	39078887	39080887	MACF1	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes	human,mouse	Bone	High+Lowthroughput	Microtubule actin crosslinking factor 1 promotes osteoblast differentiation by promoting β-catenin/TCF1/Runx2 signaling axis	否		Osteoblast differentiation	cementoblast	E_02_0047	Western blot,Real time PCR	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes		Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes	Immunohistochemical staining	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes			Western blot,Real time PCR				MACF1
28621459	chr4	108044719	108046719	LEF1	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation	human,mouse	Bone	High+Lowthroughput	Microtubule actin crosslinking factor 1 promotes osteoblast differentiation by promoting β-catenin/TCF1/Runx2 signaling axis	否		Osteoblast differentiation	cementoblast	E_02_0047	Western blot,Real time PCR	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation		It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation	Immunohistochemical staining	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation			Western blot,Real time PCR				LEF1
28462489	chr5	179729425	179731425	MAML1	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	human	Tumor	High+Lowthroughput	Role of MAML1 and MEIS1 in Esophageal Squamous Cell Carcinoma Depth of Invasion	否		esophageal squamous cell carcinoma	tumor cell	E_01_0071	qRT-PCR	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.		In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Immunohistochemical staining	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.			qRT-PCR				MAML1
28462489	chr2	66430871	66432871	MEIS1	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	human	Tumor	High+Lowthroughput	Role of MAML1 and MEIS1 in Esophageal Squamous Cell Carcinoma Depth of Invasion	否		esophageal squamous cell carcinoma	tumor cell	E_01_0071	qRT-PCR	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.		In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Immunohistochemical staining	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.			qRT-PCR				MEIS1
28442495	chr13	27958465	27960465	CDX2	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	human		High+Lowthroughput	Aspirin prevents NF-κB activation and CDX2 expression stimulated by acid and bile salts in oesophageal squamous cells of patients with Barrett's oesophagus	否		Esophageal Diseases	oesophageal squamous cell	E_01_0072	Western blot	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	Immunohistochemical staining	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	CDX2		Western blot	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.			
28115742	chr5	88714348	88716348	MEF2C	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life	human,mouse	Brain tissue	High+Lowthroughput	MEF2C transcription factor is associated with the genetic and epigenetic risk architecture of schizophrenia and improves cognition in mice	否		schizophrenia and related disorders	pluripotent stem cell	E_02_0048	ChIP-seq,ChIP-PCR	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life		However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life	Immunohistochemical staining	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life			ChIP-seq,ChIP-PCR				MEF2C
28027119	chr4	108044503	108046503	LEF1	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	human	Soft tissue	High+Lowthroughput	Comparison of β-Catenin and LEF1 Immunohistochemical Stains in Desmoid-type Fibromatosis and its Selected Mimickers, With Unexpected Finding of LEF1 Positivity in Scars	否		desmoid-type fibromatosis		E_01_0073	Immunohistochemical staining	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	Immunohistochemical staining	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	LEF1		Immunohistochemical staining	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF			
27997051	chr7	44101517	44103517	AEBP1	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes	human	Hippocampal tissue	High+Lowthroughput	Association of adipocyte enhancer-binding protein 1 with Alzheimer's disease pathology in human hippocampi	否		Alzheimer’s disease	smooth muscle cell line	E_01_0074	Western blot	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes		Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes	Immunohistochemical staining	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes			Western blot				AEBP1
27845419	chr7	87500277	87502277	ABCB1	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	human	Liver	High+Lowthroughput	ABC transporter polymorphisms are associated with irinotecan pharmacokinetics and neutropenia	是	rs12720066,rs6498588	Neutropenia	Hep G2 cell	E_01_0075	Enhancer Assay	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Immunohistochemical staining	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	ABCB1		Enhancer Assay	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.			
26842780	chr22	39517640	39519640	ATF4	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.	human,mouse	Spinal cord tissue	High+Lowthroughput	Activating Transcription Factor-6α Deletion Modulates the Endoplasmic Reticulum Stress Response after Spinal Cord Injury but Does Not Affect Locomotor Recovery	否		Spinal cord injury	Oligodendrocytes	E_02_0049	Western blot,RT-PCR	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.		While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.	Immunohistochemical staining	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.			Western blot,RT-PCR				ATF4
28860350	chr2	43219398	43221398	ZFP36L2	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor	human	Non-malignant oesophagus tissue	High+Lowthroughput	Identification of distinct mutational patterns and new driver genes in oesophageal squamous cell carcinomas and adenocarcinomas	否		Oesophageal squamous cell carcinoma (OScc) and adenocarcinoma (Oac)	squamous cell line	E_01_0076	ChIP-seq,WGBS	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor		Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor	Immunohistochemical staining	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor			ChIP-seq,WGBS				ZFP36L2
29028630	chr7	148804878	148806878	EZH2	EZH2 plays an important role in this inflammatory process of dental pulp.	human,mouse	dental pulp tissue	High+Lowthroughput	EZH2 regulates dental pulp inflammation by direct effect on inflammatory factors	否		dental pulp inflammation	dental pulp cell	E_02_0050	qPCR,ChIP,Western blot	EZH2 plays an important role in this inflammatory process of dental pulp.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 plays an important role in this inflammatory process of dental pulp.		EZH2 plays an important role in this inflammatory process of dental pulp.	Immunohistochemical staining	EZH2 plays an important role in this inflammatory process of dental pulp.			qPCR,ChIP,Western blot				EZH2
31980609	chr1	47213215	47215215	TAL1	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.	mouse	lymph	High+Lowthroughput	Interrogation of enhancer function by enhancer_x0002_targeting CRISPR epigenetic editing	否	无		K562 cell，Jurkat cell	E_02_0051	Flow cytometry, cell viability detection, QRT PCR, Western blot, RNA SEQ, chip SEQ,	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.		Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.	Immunohistochemical staining	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.			流式细胞术，细胞活力检测， qRT-PCR ，Western blot，RNA-seq，ChIP-seq，				TAL1
31980500	chr2	233757381	233759381	UGT1A1	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.	mouse	Liver, kidney	High+Lowthroughput	Differential role of LXRα and LXRβ in the regulation of UDP-glucuronosyltransferase 1A1 in humanized UGT1 mice	否	无	hepatic fibrosis 	HepG2，HK293 cell	E_02_0052	QRT PCR, Western blot, glucuronidation assay, transfection, chromatin immunoprecipitation assay, agarose gel electrophoresis	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.		An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.	Immunohistochemical staining	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.			qRT-PCR，Western Blot，葡萄糖醛酸化分析，转染，染色质免疫沉淀分析，琼脂糖凝胶电泳				UGT1A1
31975641	chr1	118880199	118882199	TBX15	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	human	bone marrow	High+Lowthroughput	Osteoporosis- and obesity-risk interrelationships: an epigenetic analysis of GWAS-derived SNPs at the developmental gene TBX15	是	Rs10494217， rs61730011，rs984222，rs1106529，rs9659323，rs12742627，, rs961470，rs17023223	Osteoporosis	cementoblast	E_01_0077	RNA SEQ, GWAS derived SNPs and LD analysis	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	Immunohistochemical staining	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	TBX15		 RNA-seq，GWAS衍生的SNPs和LD分析	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.			
31969149	chr1	8001716	8003716	ERRFI1	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 	human	lung	High+Lowthroughput	An integrated analysis of public genomic data unveils a possible functional mechanism of psoriasis risk via a long-range ERRFI1 enhancer	是	rs72635708	psoriasis	IMR-90 cell	E_01_0078	ChIP-seq	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 		 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 	Immunohistochemical staining	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 			ChIP-seq				ERRFI1
31968281	chr16	88712787	88714787	PIEZO1	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.	mouse	bone marrow	High+Lowthroughput	Identification of PIEZO1 polymorphisms for human bone mineral density	是	rs62048221	Osteoporotic fracture	mesenchymal stem cell	E_02_0053	Luciferase reporter assay, chip qPCR	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.		Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.	Immunohistochemical staining	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.			荧光素酶报告分析，ChIP-qPCR 				PIEZO1
31967103	chr7	148804333	148806333	EZH2	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	human	kidney	High+Lowthroughput	Site-directed targeting of transcriptional activation-associated proteins to repressed chromatin restores CRISPR activity	否	无		HEK293 cell	E_01_0079	Transfection, luciferase assay, flow cytometry, chip qPCR,	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	Immunohistochemical staining	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	EZH2		转染，荧光素酶分析，流式细胞术，ChIP-qPCR，	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 			
31963554	chr10	52311442	52313442	DKK1	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.	human	Bone, mesenchymal tissue	High+Lowthroughput	DKK1 Induced by 1,25D3 Is Required for the Mineralization of Osteoblasts	否	无	Osteoporosis	osteogenitorcell,cementoblast，SaOS2 cell	E_01_0080	QPCR, Western blot, immunofluorescence, luciferase assay, chromatin immunoprecipitation assay	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.		Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.	Immunohistochemical staining	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.			qPCR，Western Blot，免疫荧光，荧光素酶分析，染色质免疫沉淀分析				DKK1
31961892	chr11	55334650	55336650	Atox1	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	human	colon	High+Lowthroughput	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	否	无	Colon cancer	SW480 cell	E_01_0081	Immunofluorescence, Western blot, transfection, cell colony assay	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer		Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	Immunohistochemical staining	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer			免疫荧光，Western blot，转染，细胞集落实验				Atox1
31954402	chr7	148804633	148806633	EZH2	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	human	blood	High+Lowthroughput	Differential expression of microRNA, miR-150 and enhancer of zeste homolog 2 (EZH2) in peripheral blood cells as early prognostic markers of severe forms of dengue	否	无	dengue fever		E_01_0082	qRT-PCR	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	Immunohistochemical staining	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	EZH2		qRT-PCR	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.			
31953940	chr4	108045068	108047068	LEF1	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	human		High+Lowthroughput	Immunohistochemical Expression of Lymphoid Enhancer Binding Factor 1 in CD5-Positive Marginal Zone, Lymphoplasmacytic, and Follicular Lymphomas.	否	无	Lymphoplasmacytoma, follicular lymphoma	tumor cell	E_01_0083	Immunohistochemistry, flow cytometry, fluorescence in situ hybridization, QRT PCR	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	Immunohistochemical staining	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	LEF1		免疫组化，流式细胞术，荧光原位杂交技术，qRT-PCR	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.			
31953319	chr22	39516679	39518679	ATF4	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	human	skeletal muscle	High+Lowthroughput	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ	否	无	Skeletal muscle atrophy	mouse cell of skeletal muscle	E_01_0084	Western blot, transfection, qPCR, agarose gel electrophoresis	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	Immunohistochemical staining	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	ATF4		Western Blot，转染，qPCR，琼脂糖凝胶电泳	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.			
31952907	chr7	148804371	148806371	EZH2	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	human	Connective tissue, peripheral blood	High+Lowthroughput	EZH2 deficiency attenuates Treg differentiation in rheumatoid arthritis	否	无	Rheumatoid arthritis	synovial cell，peripheral blood mononuclear cell，Jurkat T cell	E_01_0085	Western blot，RT-qPCR	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	Immunohistochemical staining	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	EZH2		Western blot，RT-qPCR	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.			
31951295	chr15	88633030	88635030	ISG20	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.	human	liver	High+Lowthroughput	Antiviral activity of interferon-stimulated gene 20, as a putative repressor binding to hepatitis B virus enhancer II and core promoter	否	无	hepatitis B	HepG2，HepG2 NTCP，HepAD38 cell	E_01_0086	Immunohistochemistry, luciferase analysis, transfection, Southern blot, Northern blot, Western blot, RT-PCR, chromatin immunoprecipitation analysis, microarray data analysis	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.		Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.	Immunohistochemical staining	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.			免疫组化，荧光素酶分析，转染，Southern blot ，Northern blot，Western  blot，RT-PCR ，染色质免疫沉淀分析，微阵列数据分析				ISG20
31938642	chr9	81581120	81583120	TLE1	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	human		High+Lowthroughput	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	否	无	Soft tissue sarcoma		E_01_0087	Immunohistochemistry	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	Immunohistochemical staining	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	TLE1		免疫组化	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study			
31937792	chr9	78383023	78385023	Eef1a1	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.	mouse	embryo	High+Lowthroughput	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus	否	无	tumour	embryonic stem cell	E_02_0054	Immunofluorescence, immunohistochemistry, he staining, Southern blot, PCR	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.		Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.	Immunohistochemical staining	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.			免疫荧光，免疫组化，HE染色，Southern blot，PCR				Eef1a1
31937612	chr5	69232027	69234027	CDK7	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	human	bone	High+Lowthroughput	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	否	无	Osteosarcoma	SJSA-1 cell，U2-OS cell，HOS cell，G-292 cell，MNNG/HOS cell，143B cell，MG-63 cell，cementoblast	E_01_0088	Chromatin immunoprecipitation, microarray, transfection, cell viability assay, Transwell, Western blot, RT qPCR	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor		Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	Immunohistochemical staining	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor			染色质免疫沉淀，微阵列，转染，细胞活力检测，Transwell，Western blot，RT-qPCR				CDK7
31933869	chr11	113406893	113408893	DRD2	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.	human	Peripheral blood	High+Lowthroughput	Functional tag SNPs inside the DRD2 gene as a genetic risk factor for major depressive disorder in the Chinese Han population	是	rs4648317，rs7131056	Major depressive disorder	peripheral blood mononuclear cell	E_01_0089	PCR	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.		This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.	Immunohistochemical staining	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.			PCR				DRD2
31933740	chr9	81580946	81582946	TLE1	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	human		High+Lowthroughput	Transducer-like enhancer of split 1 (TLE1) as a novel biomarker for diagnosis of synovial sarcoma correlates with translocation t(X;18): a study of 155 cases in China	否	无	Synovial sarcoma		E_01_0090	Immunohistochemistry, fluorescence in situ hybridization	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	Immunohistochemical staining	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	TLE1		免疫组化，荧光原位杂交	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.			
31932307	chr20	21508188	21510188	NKX2-2	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	mouse	brain	High+Lowthroughput	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	否	无		CG4 cell	E_02_0055	In situ hybridization, immunohistochemistry, immunofluorescence, CO immunoprecipitation, Western blot	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors		The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	Immunohistochemical staining	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors			原位杂交，免疫组化，免疫荧光，免疫共沉淀，Western blot				NKX2-2
31929803	chr4	108044497	108046497	LEF1	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	human		High+Lowthroughput	Prognostic Impact of Lymphoid Enhancer Factor 1 Expression and Serum Galectin.3 in Egyptian AML Patients	否	无	Acute myeloid leukemia		E_01_0091	RT qPCR, ELISA	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	Immunohistochemical staining	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	LEF1		RT-qPCR，联酶免疫吸附反应	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.			
31928966	chr6	10978082	10980082	ELOVL2	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	human	liver	High+Lowthroughput	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	是	rs953413	liver cancer	HepG2 cell	E_01_0092	As qPCR, chip SEQ, gene knockdown, QRT PCR, chromatin immunoprecipitation, luciferase reporter	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression		rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	Immunohistochemical staining	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression			AS-qPCR，ChIP-seq，基因敲除，qRT-PCR，染色质免疫沉淀，荧光素酶报告基因				ELOVL2
31927142	chr22	28791896	28793896	XBP1	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.	mouse	kidney	High+Lowthroughput	X-box binding protein 1 (XBP1): A key protein for renal osmotic adaptation. Its role in lipogenic program regulation	否	无		MDCK cell	E_02_0056	Transfection, RT-PCR, Western blot, immunofluorescence	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.		Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.	Immunohistochemical staining	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.			转染，RT-PCR，Western blot，免疫荧光				XBP1
31915257	chr11	27652693	27654693	BDNF	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	mouse	brain	High+Lowthroughput	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	否	无			E_02_0057	RT qPCR, luciferase reporter assay, Western blot, immunocytochemistry, chromatin immunoprecipitation	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons		CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	Immunohistochemical staining	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons			RT-qPCR ，荧光素酶报告试验，Western blot，免疫细胞化学，染色质免疫沉淀				BDNF
31914694	chr7	148804420	148806420	EZH2	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.	mouse	kidney	High+Lowthroughput	Enhancer of zeste homolog 2 modulates oxidative stress-mediated pyroptosis in vitro and in a mouse kidney ischemia-reperfusion injury model	否	无	Renal ischemia reperfusion injury	HK-2 cell	E_02_0058	RT-PCR, Western blot, he staining, immunohistochemistry, TUNEL staining, cell viability assay, luciferase reporter assay, transfection, immunofluorescence	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.		 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.	Immunohistochemical staining	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.			RT-PCR，Western blot，HE染色，免疫组化，TUNEL染色，细胞活力检测，荧光素酶报告分析，转染，免疫荧光				EZH2
31914533	chr19	19142448	19144448	MEF2B	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 	human		High+Lowthroughput	Expression of myocyte enhancer factor 2B in mantle cell lymphoma and its clinical significance	否	无	Mantle cell lymphoma		E_01_0093	He staining, immunohistochemistry, fluorescence in situ hybridization	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 		The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 	Immunohistochemical staining	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 			HE染色，免疫组化，荧光原位杂交				MEF2B
31914083	chr5	51380063	51382063	ISL1	ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	human		High+Lowthroughput	Correlations between ISL1 rs1017 polymorphism and congenital heart disease risk: A PRISMA-compliant meta-analysis	是	rs1017	Congenital heart disease	cardiac muscle cell (sensu Arthopoda)	E_01_0094		ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	Immunohistochemical staining	ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	ISL1			ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.			
31910882	chr11	306685	308685	IFITM1	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 	human	bone marrow	High+Lowthroughput	Epigenetic regulation of IFITM1 expression in lipopolysaccharide-stimulated human mesenchymal stromal cells	否	无		hMSC cell	E_01_0095	QRT PCR, ELISA, Western blot, immunocytochemistry, chromatin immunoprecipitation PCR, chip SEQ, scratch assay, gene knockdown, luciferase reporter assay	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 		Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 	Immunohistochemical staining	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 			qRT-PCR，酶联免疫吸附试验，Western blot，免疫细胞化学，染色质免疫沉淀PCR，ChIP-seq，划痕实验，基因敲降，荧光素酶报告试验				IFITM1
31909872	chr5	177129035	177131035	NSD1	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.	mouse		High+Lowthroughput	Investigating cortical features of Sotos syndrome using mice heterozygous for Nsd1.	否	无	Sotos syndrome		E_02_0059	Immunofluorescence, genotyping PCR, qPCR, hematoxylin staining,	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.		We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.	Immunohistochemical staining	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.			免疫荧光，基因分型PCR，qPCR，苏木精染色，				NSD1
31908011	chr2	199267108	199269108	SATB2	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.	mouse	Cord blood, skull	High+Lowthroughput	Maternal regulation of SATB2 in osteo-progeniters impairs skeletal development in offspring	否	无	Skeletal development	mesenchymal stem cell，skull cells	E_02_0060	Immunohistochemistry, chromatin immunoprecipitation, chip SEQ, RT qPCR, Western blot	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.		These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.	Immunohistochemical staining	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.			免疫组化，染色质免疫沉淀，ChIP-seq，RT-qPCR，Western blot				SATB2
31902945	chr22	27745785	27747785	MN1	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	human	bone marrow	High+Lowthroughput	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	否	无	Myeloid neoplasms	Bone marrow monocytes	E_01_0096	Whole genome sequencing, RT-PCR, fluorescence in situ hybridization, Sanger sequencing	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)		Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	Immunohistochemical staining	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)			全基因组测序，RT-PCR，荧光原位杂交，sanger测序				MN1
31900258	chr5	1250197	1252197	TERT	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	human		High+Lowthroughput		否	无	Neuroblastoma	neuroblastoma cells，SK-N-AS cell	E_01_0097	Chip – qPCR, RT qPCR, Western blot, cell viability assay	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	Immunohistochemical staining	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	TERT		ChIP–qPCR，RT-qPCR，Western blot，细胞活力检测	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.			
31899875	chr14	100776332	100778332	MEG3	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.	human	ovarian follicle	High+Lowthroughput	MEG3/MIR-376B-3P/HMGA2 axis is involved in pituitary tumor invasiveness	否	无	Pituitary tumors		E_01_0098	Dual luciferase reporter assay, immunofluorescence, IHC, RT qPCR, Western blot, flow cytometry, TUNEL staining, transfection, cell viability assay, Transwell, scratch assay	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.		Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.	Immunohistochemical staining	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.			双荧光素酶报告基因，免疫荧光，，免疫组化，RT-qPCR，Western blot，流式细胞术，TUNEL染色，转染，细胞活力检测，Transwell，划痕实验				MEG3
31897846	chr19	2974615	2976615	TLE6	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	human		High+Lowthroughput	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	否	无	Infertility		E_01_0099	Whole exome sequencing, Sanger sequencing	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations		Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	Immunohistochemical staining	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations			全外显子组测序，Sanger测序				TLE6
31897220	chr1	6098734	6100734	CHD5	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.	human	Stomach, cervix	High+Lowthroughput	Clinical significance of chromatin remodeling factor CHD5 expression in gastric cancer	否	无	gastric cancer	AGS cell, KATO III cell, MKN45 cell, NCI-N87 cell, NUGC-3 cell, OCUM‑1 cell,HeLa cell 	E_01_0100	Immunohistochemistry, scratch assay, cell viability assay, Transwell, Western blot, RT ＾ PCR	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.		In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.	Immunohistochemical staining	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.			免疫组化，划痕实验，细胞活力检测，Transwell，western blot，RT‑PCR				CHD5
31897216	chr4	7751333	7753333	AFAP1-AS1	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.	human	lung	High+Lowthroughput	AFAP1-AS1 induces cisplatin resistance in non-small cell lung cancer through PI3K/AKT pathway	否	无	Non small cell lung cancer	A549 cell	E_01_0101	RNA immunoprecipitation, flow cytometry, Western blot, Transwell, RT ‐qpcr	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.		 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.	Immunohistochemical staining	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.			RNA免疫沉淀，流式细胞术，Western blot，Transwell，RT‑qPCR				AFAP1-AS1
31893185	chr9	81580729	81582729	TLE1	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	human		High+Lowthroughput	Is TLE1 Expression Limited to Synovial Sarcoma? Our Experience at Shifa International Hospital, Pakistan	否	无	Synovial sarcoma		E_01_0102	Immunohistochemistry	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	Immunohistochemical staining	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	TLE1		免疫组化	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.			
31892537	chr10	102103573	102105573	LDB1	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.	human	blood	High+Lowthroughput	Crystal structure of human LDB1 in complex with SSBP2	否	无		erythrocyte	E_01_0103	pull-down	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.		Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.	Immunohistochemical staining	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.			pull-down				LDB1
31891591	chr7	148804482	148806482	EZH2	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	human		High+Lowthroughput	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	否	无	epilepsy		E_01_0104	Western blot，qRT-PCR，LC-MS	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	Immunohistochemical staining	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	EZH2		Western blot，qRT-PCR，LC-MS	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy			
31890812	chr2	60447611	60449611	BCL11A	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.	human	Kidney, peripheral blood, bone marrow	High+Lowthroughput	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion	否	无	β- Thalassemia disorders	HEK293T cell， KU812 cell，KG-1 cell	E_01_0105	Agarose gel electrophoresis, QRT PCR	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.		Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.	Immunohistochemical staining	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.			琼脂糖凝胶电泳， qRT-PCR				BCL11A
31888703	chr3	12284215	12286215	PPARG	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	human		High+Lowthroughput	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	是	 rs10865710	Traumatic sepsis		E_01_0106	Western blot, dual luciferase gene reporter	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	Immunohistochemical staining	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	PPARG		Western blot，双荧光素酶基因报告	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression			
31886719	chr11	100684149	100686149	ARHGAP42	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.	human	Aortic smooth muscle, bronchial smooth muscle	High+Lowthroughput	Transcriptional and posttranscriptional regulation of the SMC-selective blood pressure-associated gene, ARHGAP42	是	rs604723	Blood pressure regulation	HUAOSMC cell，HUBRSMC cell	E_01_0107	Luciferase assay, immunoprecipitation, QRT PCR, chromatin immunoprecipitation assay, Western blot, electrophoretic mobility shift assay, immunofluorescence	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.		First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.	Immunohistochemical staining	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.			荧光素酶分析，免疫沉淀，qRT-PCR，染色质免疫沉淀实验，Western blot，电泳迁移率分析，免疫荧光				ARHGAP42
31886200	chr7	148804829	148806829	EZH2	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	human	bone marrow	High+Lowthroughput	Aberrant Expression of EZH2 in Pediatric Patients with Myelodysplastic Syndrome: A Potential Biomarker of Leukemic Evolution	否	无	Pediatric myelodysplastic syndrome	bone marrow cell	E_01_0108	qRT–PCR	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	Immunohistochemical staining	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	EZH2		qRT–PCR	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.			
31882553	chr19	15232668	15234668	BRD4	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	human	lymph	High+Lowthroughput	BRD4-Regulated Molecular Targets in Mantle Cell Lymphoma: Insights into Targeted Therapeutic Approach	否	无	Mantle cell lymphoma	JVM-2 cell，MINO cell，Z138 cell，KPUM-YY1 cell	E_01_0109	Cell viability assay, Western blot, QRT PCR, chromatin immunoprecipitation	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	Immunohistochemical staining	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	BRD4		细胞活力检测，Western blot，qRT-PCR，染色质免疫沉淀	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.			
31878072	chr1	153659104	153661104	ILF2	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.	human	Kidney, peripheral blood	High+Lowthroughput	Enterovirus 71 Represses Interleukin Enhancer-Binding Factor 2 Production and Nucleus Translocation to Antagonize ILF2 Antiviral Effects	否	无	antiviral	HEK293T cell、Vero cell、RD cell，thp-1 cell	E_01_0110	RT qPCR, Western blot, CO immunoprecipitation, immunofluorescence	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.		Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.	Immunohistochemical staining	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.			RT-qPCR，Western blot，免疫共沉淀，免疫荧光				ILF2
31866294	chr7	148804551	148806551	EZH2	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	human	colon	High+Lowthroughput	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2	否	无	tumour	HCT116 cell	E_01_0111	Fluorescence polarization assay, Western blot, CO immunoprecipitation	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	Immunohistochemical staining	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	EZH2		荧光偏振分析，Western Blot，共免疫沉淀	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.			
31866047	chr20	59860441	59862441	SYCP2	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	human	lymph	High+Lowthroughput	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	是	 rs568645874， rs199662252，rs45568532, rs551180067,  rs11549332		Lymphoblast	E_01_0112	QRT PCR, Western blot, Sanger sequencing, PAS staining, hematoxylin staining	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility		SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	Immunohistochemical staining	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility			qRT-PCR，Western Blot，Sanger测序，PAS染色，苏木精染色				SYCP2
31865141	chr3	3142136	3144136	CRBN	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.	mouse	lung	High+Lowthroughput	CRBN knockdown mitigates lipopolysaccharide-induced acute lung injury by suppression of oxidative stress and endoplasmic reticulum (ER) stress associated NF-κB signaling	否	无	acute lung injury 	A549 cell	E_02_0061	Biochemical analysis, he staining, immunofluorescence, ELISA, Western blot, QRT PCR, intracellular reactive oxygen species detection	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.		In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.	Immunohistochemical staining	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.			生化分析，HE染色，免疫荧光，ELISA，Western blot，qRT-PCR，细胞内活性氧检测				CRBN
31864713	chr7	44101569	44103569	AEBP1	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	human	brain	High+Lowthroughput	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	否	无	Gliomas	U87MG cell，U251 MG cell	E_01_0113	Western blot, immunohistochemistry, QRT PCR, cell viability assay, Transwell, immunofluorescence, flow cytometry	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis		Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	Immunohistochemical staining	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis			Western-blot，免疫组化，qRT-PCR，细胞活力检测，Transwell，免疫荧光，流式细胞术				AEBP1
31861475	chr9	36570240	36572240	MELK	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	human	bile duct	High+Lowthroughput	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	否	无	Intrahepatic cholangiocarcinoma	iCCA cell	E_01_0114	RT-PCR, immunohistochemistry	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma		Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	Immunohistochemical staining	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma			RT-PCR，免疫组织化学				MELK
31860165	chr4	52709533	52711533	DANCR	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	human	breast	High+Lowthroughput	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	否	无	mammary cancer	breast cancer cells，mammary gland epithelial cell	E_01_0115	QRT PCR, cell viability assay, ELISA, Western blot, RNA immunoprecipitation, chromatin immunoprecipitation, Transwell	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription		The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	Immunohistochemical staining	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription			qRT-PCR，细胞活力检测，ELISA，Western blot，RNA免疫沉淀，染色质免疫沉淀，Transwell				DANCR
31858612	chr14	53946742	53948742	BMP4	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.	mouse	bone marrow	High+Lowthroughput	Effect of GSK-137647A, the first non-carboxylic FFA4 agonist, on the osteogenic and adipogenic differentiation of bone mesenchymal stem cells in db/db mice	否	无		mesenchymal stem cell of the bone marrow，cementoblast	E_02_0062	Flow cytometry, cell viability assay, oil red O staining, Western blot, RT qPCR	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.		The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.	Immunohistochemical staining	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.			流式细胞术，细胞活力检测，油红O染色，Western blot，RT-Qpcr				BMP4
31858557	chr15	42735912	42737912	TTBK2	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	human	brain	High+Lowthroughput	Circular RNA TTBK2 promotes the development of human glioma cells via miR-520b/EZH2 axis	否	无	Gliomas	A172 cell，U251 cell，astrocyte cell	E_01_0116	Transfection, QRT PCR, Western blot, flow cytometry, Transwell, dual luciferase reporter assay	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	Immunohistochemical staining	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	TTBK2		转染，qRT-PCR，Western Blot，流式细胞术，Transwell，双荧光素酶报告分析	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.			
31856860	chr20	50188118	50190118	CEBPB	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	human		High+Lowthroughput	A longitudinal study highlights shared aspects of the transcriptomic response to cardiogenic and septic shock	否	无	Cardiogenic and septic shock		E_01_0117	RNA sequencing	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	Immunohistochemical staining	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	CEBPB		RNA测序	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.			
31851943	chr19	1606379	1608379	TCF3	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	human	bone marrow	High+Lowthroughput	Spatial Genome Re-organization between Fetal and Adult Hematopoietic Stem Cells	否	无		HPC-7 cell	E_01_0118	Dna-fish, Western blot, flow cytometry	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	Immunohistochemical staining	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	TCF7L1		DNA-FISH， Western blot，流式细胞术	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.			
31845224	chr2	26345405	26347405	Notch1	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.	human	gallbladder	High+Lowthroughput	Notch1 Drives the Formation and Proliferation of Intrahepatic Cholangiocarcinoma	否	无	Intrahepatic cholangiocarcinoma	BC-939 cell，RBE cell	E_01_0119	Western blot, flow cytometry, Western blot, immunohistochemistry, immunofluorescence, QRT PCR	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.		Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.	Immunohistochemical staining	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.			Western blot， 流式细胞术，Western Blot，免疫组化，免疫荧光，qRT-PCR				Notch1
31845180	chr8	81475612	81477612	FABP4	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	mouse		High+Lowthroughput	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	否	无		3T3-LL cell	E_02_0063	Oil red O staining, Western blot	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes		Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	Immunohistochemical staining	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes			油红O染色，Western blot				FABP4
31844321	chr5	129458078	129460078	ADAMTS19	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.	mouse	valve	High+Lowthroughput	Loss of ADAMTS19 causes progressive non-syndromic heart valve disease	否	无	Valvular heart disease	valve interstitial cells	E_02_0064	Immunohistochemistry, immunofluorescence,	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.		Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.	Immunohistochemical staining	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.			免疫组化，免疫荧光，				ADAMTS19
31843716	chr18	55219904	55221904	TCF4	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	human	breast	High+Lowthroughput	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	否	无	mammary cancer	MCF-7 cell，MDA-MB-231 cell	E_01_0120	Flow cytometry, immunofluorescence, Western blot	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	Immunohistochemical staining	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	TCF4		流式细胞术，免疫荧光，Western blot	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells			
31843273	chr7	148804648	148806648	EZH2	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	human		High+Lowthroughput	Overexpression of enhance of Zeste homolog 2 (EZH2) in endometrial carcinoma: An NRG Oncology/Gynecologic Oncology Group Study	否	无	Endometrial cancer		E_01_0121	RT-PCR，Western blot	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	Immunohistochemical staining	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	EZH2		RT-PCR，Western blot	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.			
31841397	chr7	148804351	148806351	EZH2	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	mouse	uterus	High+Lowthroughput	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	否	无	Uterine epithelial VAS	epithelial cell of uterus	E_02_0065	Immunohistochemistry, qPCR	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation		Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	Immunohistochemical staining	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation			免疫组化，qPCR				EZH2
31840569	chr17	80542354	80544354	RPTOR	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.	mouse	Fat	High+Lowthroughput	Sustained activation of autophagy suppresses adipocyte maturation via a lipolysis-dependent mechanism	否	无		fat cell	E_02_0066	Immunofluorescence, flow cytometry, oil red O staining, he staining, immunohistochemistry, Western blot	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.		Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.	Immunohistochemical staining	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.			免疫荧光，流式细胞术，油红O染色，HE染色，免疫组化，western blot 				RPTOR
31836590	chr1	145918614	145920614	RBM8A	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 	human		High+Lowthroughput	1q21.1 deletion and a rare functional polymorphism in siblings with thrombocytopenia-absent radius-like phenotypes	是	rs61746197	Thrombocytopenia, radial hypoplasia		E_01_0122	Western blot	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 		Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 	Immunohistochemical staining	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 			Western blot				RBM8A
31833556	chr7	148804595	148806595	EZH2	By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 	mouse		High+Lowthroughput	Transcription Factor Enrichment Analysis in Enhancers Identifies EZH2 as a Susceptibility Gene for Osteoporosis	是	rs111851041	Osteoporosis		E_02_0067		By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 		By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 	Immunohistochemical staining	By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 							EZH2
31831267	chr7	148804596	148806596	EZH2	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	human	Cervix, lymph, kidney	High+Lowthroughput	Degradation of Polycomb Repressive Complex 2 with an EED-Targeted Bivalent Chemical Degrader	否	无	cancer	Hela cell，DB cell，Pfeiffer cell，293T Cell 	E_01_0123	Western blot, cell viability assay	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	Immunohistochemical staining	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	EZH2		Western Blot，细胞活力检测	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.			
31827084	chrX	113613674	113615674	XACT	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.	human	embryo	High+Lowthroughput	A primate-specific retroviral enhancer wires the XACT lncRNA into the core pluripotency network in humans	否	无		embryonic stem cell	E_01_0124	Rna-fish, RT qPCR, chromatin immunoprecipitation, Western blot,	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.		This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.	Immunohistochemical staining	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.			RNA-FISH，RT-qPCR，染色质免疫沉淀，western blot，				XACT
31826955	chr14	37586693	37588693	FOXA1	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	human	breast	High+Lowthroughput	FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer	否	无	mammary cancer	MCF7L cell，T47D cell，600MPE cell	E_01_0125	Western blot, immunohistochemistry, QRT PCR	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	Immunohistochemical staining	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	FOXA1		Western blot，免疫组化，qRT-PCR	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.			
31825847	chr20	64045290	64047290	SOX18	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	human	ovary	High+Lowthroughput	A Study of High-Grade Serous Ovarian Cancer Origins Implicates the SOX18 Transcription Factor in Tumor Development	否	无	oophoroma	FT246，FT282，FT318，CaOV3，COV318，EFO21，Kuramochi，FUOV1，OAW28，OV177，OVSAHO，TykNu，UWB1.289 cell	E_01_0126	western blot，qRT-PCR	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	Immunohistochemical staining	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	SOX18		western blot，qRT-PCR	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.			
31819273	chr7	148804439	148806439	EZH2	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	human	breast	High+Lowthroughput	Discovery of a first-in-class EZH2 selective degrader	否	无	cancer	MDA-MB-231，MDA-MB-468，BT549	E_01_0127	Western blot, cell viability assay, crystal violet staining, QRT PCR	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	Immunohistochemical staining	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	EZH2		western blot，细胞活力检测，结晶紫染色，qRT-PCR	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.			
31817839	chr1	115283204	115285204	NGF	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	human	ovary	High+Lowthroughput	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	否	无	Epithelial ovarian cancer	HOSE cell，A2780 cell，SKOV3 cell，OV90 cell，NIH-OVCAR3 cell	E_01_0128	Immunohistochemistry, immunocytochemistry, Western blot, QRT PCR, ELISA	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis		NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	Immunohistochemical staining	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis			免疫组织化学，免疫细胞化学，Western Blot，qRT-PCR， ELISA				NGF
31815603	chr6	133886394	133888394	TCF21	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.	mouse	coronary artery	High+Lowthroughput	Coronary Disease-Associated Gene TCF21 Inhibits Smooth Muscle Cell Differentiation by Blocking the Myocardin-Serum Response Factor Pathway	否	无	coronary artery disease 	smooth muscle cell	E_02_0068	Western blot, chromatin immunoprecipitation sequencing, transfection	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.		These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.	Immunohistochemical staining	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.			Western Blot，染色质免疫沉淀测序，转染				TCF21
31804013	chr5	151027281	151029281	TNIP1	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	human	Peripheral blood	High+Lowthroughput	Role of Systemic Lupus Erythematosus Risk Variants With Opposing Functional Effects as a Driver of Hypomorphic Expression of TNIP1 and Other Genes Within a Three-Dimensional Chromatin Network	否	无	Systemic lupus erythematosus	Jurkat cell，THP-1cell	E_01_0129	Dual luciferase reporter assay, electrophoretic mobility shift assay, QRT PCR, Western blot, and pulldown	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	Immunohistochemical staining	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	TNIP1		双荧光素酶报告分析，电泳迁移率分析，qRT-PCR，Western blot，pulldown 	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.			
31799674	chr12	53959218	53961218	HOTAIR	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	human	bone marrow	High+Lowthroughput	Effects of lncRNA HOTAIR on proliferation and apoptosis of myeloma cells through NF-κB pathway	否	无	Myeloma	Myeloma cell	E_01_0130	QRT PCR, flow cytometry, Western blot, cell viability assay, transfection	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	Immunohistochemical staining	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	HOTAIR		qRT-PCR，流式细胞术，Western blot，细胞活力检测，转染	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.			
31786140	chr7	27195600	27197600	HOTTIP	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	mouse	Kidney, bone marrow	High+Lowthroughput	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	否	无	Acute myeloid leukemia	HEK293T cell，OCI-AML3 cell	E_02_0069	QRT PCR, rip, flow cytometry, chromatin immunoprecipitation	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice		HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	Immunohistochemical staining	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice			qRT-PCR，RIP，流式细胞术，染色质免疫沉淀				HOTTIP
33081480	chr18	47806258	47808258	SMAD2	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).	mouse	brain tissue	High+Lowthroughput	The inhibitory effect of Gualou Guizhi Decoction on post-ischemic neuroinflammation via miR-155 in MCAO rats	否		stroke	Inflammatory cell	E_02_0070	RT-qPCR，Western blot，Immunohistochemistry	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).		GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).	Immunohistochemical staining	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).			RT-qPCR，Western blot，Immunohistochemistry				SMAD2
29861522	chr3	149159891	149161891	CP	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	mouse	Epithelial tissues	High+Lowthroughput	Effect of diethyldithiocarbamate in cyclophosphamide-induced nephrotoxicity: Immunohistochemical study of superoxide dismutase 1 in rat	否		Renal impairment	nephron tubule epithelial cell	E_02_0071	Biochemical analyses,Immunohistochemistry	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.		The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Immunohistochemical staining	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.			Biochemical analyses,Immunohistochemistry				CP
29861522	chr21	31656571	31658571	SOD1	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	mouse	Epithelial tissues	High+Lowthroughput	Effect of diethyldithiocarbamate in cyclophosphamide-induced nephrotoxicity: Immunohistochemical study of superoxide dismutase 1 in rat	否		Renal impairment	nephron tubule epithelial cell	E_02_0071	Biochemical analyses,Immunohistochemistry	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.		The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Immunohistochemical staining	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.			Biochemical analyses,Immunohistochemistry				SOD1
29861296	chr18	26013138	26015138	SS18	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	human	Synovial sarcoma tissues	High+Lowthroughput	The SS18-SSX Fusion Oncoprotein Hijacks BAF Complex Targeting and Function to Drive Synovial Sarcoma	否		Synovial sarcoma (SS)	HEK293T LentiX cell	E_01_0131	Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.		These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Immunohistochemical staining	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.			Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors				SS18
29861296	chr22	23783961	23785961	SMARCB1	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	human	Synovial sarcoma tissues	High+Lowthroughput	The SS18-SSX Fusion Oncoprotein Hijacks BAF Complex Targeting and Function to Drive Synovial Sarcoma	否		Synovial sarcoma (SS)	HEK293T LentiX cell	E_01_0131	Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.		These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Immunohistochemical staining	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.			Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors				SMARCB1
29859467	chr10	67881752	67883752	SIRT1	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	mouse	Epididymal white adipose tissue	High+Lowthroughput	Qing Gan Zi Shen Tang alleviates adipose tissue dysfunction with up-regulation of SIRT1 in spontaneously hypertensive rat	否		Hypertension, obesity, hyperlipidemia, insulin resistance	fat cell	E_02_0072	ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.		Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Immunohistochemical staining	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.			ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC				SIRT1
29859467	chr13	40553149	40555149	FOXO1	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	mouse	Epididymal white adipose tissue	High+Lowthroughput	Qing Gan Zi Shen Tang alleviates adipose tissue dysfunction with up-regulation of SIRT1 in spontaneously hypertensive rat	否		Hypertension, obesity, hyperlipidemia, insulin resistance	fat cell	E_02_0072	ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.		Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Immunohistochemical staining	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.			ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC				FOXO1
29859467	chr8	81475508	81477508	FABP4	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	mouse	Epididymal white adipose tissue	High+Lowthroughput	Qing Gan Zi Shen Tang alleviates adipose tissue dysfunction with up-regulation of SIRT1 in spontaneously hypertensive rat	否		Hypertension, obesity, hyperlipidemia, insulin resistance	fat cell	E_02_0072	ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.		Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Immunohistochemical staining	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.			ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC				FABP4
29859124	chr1	11009935	11011935	TARDBP	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.	human	Nervous tissue	High+Lowthroughput	Protective paraspeckle hyper-assembly downstream of TDP-43 loss of function in amyotrophic lateral sclerosis	否		Amyotrophic lateral sclerosis (ALS)	SH-SY5Y neuroblastoma cell	E_01_0132	Immunocytochemistry,RNA-FISH,RIP,PCR,Western blot,qRT-PCR,Real-time qPCR,transfection,Cell Viability Assay	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.		Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.	Immunohistochemical staining	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.			Immunocytochemistry,RNA-FISH,RIP,PCR,Western blot,qRT-PCR,Real-time qPCR,transfection,Cell Viability Assay				TARDBP
31484726	chr12	53959112	53961112	HOTAIR	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.	human,mouse		High+Lowthroughput	Comprehensive analysis of long noncoding RNA (lncRNA)-chromatin interactions reveals lncRNA functions dependent on binding diverse regulatory elements	否		cervical carcinoma	HeLa-S3 cell	E_02_0073	PCR,Flow cytometry	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.		Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.	Immunohistochemical staining	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.			PCR,Flow cytometry				HOTAIR
31484079	chr7	150942398	150944398	KCNH2	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.	human,mouse	liver	High+Lowthroughput	Identification and Characterization of a Transcribed Distal Enhancer Involved in Cardiac Kcnh2 Regulation	是	rs9640171	liver cancer	hepatocellular carcinoma derived cell	E_02_0074	PCR,Flow cytometry	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.		The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.	Immunohistochemical staining	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.			PCR,Flow cytometry				KCNH2
32517740	chr4	153777966	153779966	SFRP2	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.	human		High+Lowthroughput	Association between variation of circulating 25-OH vitamin D and methylation of secreted frizzled-related protein 2 in colorectal cancer	否		Colorectal cancer	Human colorectal carcinoma cell	E_01_0133	PCR	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.		We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.	Immunohistochemical staining	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.			PCR				SFRP2
32517078	chr10	112947720	112949720	TCF7L2	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	human		High+Lowthroughput	Embryonic Program Activated during Blast Crisis of Chronic Myelogenous Leukemia (CML) Implicates a TCF7L2 and MYC Cooperative Chromatin Binding	否		Chronic Myelogenous Leukemia	K562 cell	E_01_0134	QRT-PCR，	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	Immunohistochemical staining	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	TCF7L2		QRT-PCR，	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.			
32514254	chr12	56749082	56751082	HSD17B6	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.	human		High+Lowthroughput	Downexpression of HSD17B6 correlates with clinical prognosis and tumor immune infiltrates in hepatocellular carcinoma	否		Hepatocellular carcinoma	HCC cell	E_01_0135	Gene set enrichment analysis，RT‑qPCR，Western blot	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.		HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.	Immunohistochemical staining	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.			Gene set enrichment analysis，RT‑qPCR，Western blot				HSD17B6
29945972	chrX	49025737	49027737	TFE3	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	human,mouse		High+Lowthroughput	Protein phosphatase 2A stimulates activation of TFEB and TFE3 transcription factors in response to oxidative stress	否		cancer		E_02_0075	Western blot, immunofluorescence staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.		The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Immunohistochemical staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.			western blot,免疫荧光染色				TFE3
29945972	chr14	105848654	105850654	IGHM	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	human,mouse		High+Lowthroughput	Protein phosphatase 2A stimulates activation of TFEB and TFE3 transcription factors in response to oxidative stress	否		cancer		E_02_0075	Western blot, immunofluorescence staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.		The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Immunohistochemical staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.			western blot,免疫荧光染色				IGHM
29945888	chr11	120233455	120235455	POU2F3	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	POU2F3		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945888	chr12	102954806	102956806	ASCL1	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	ASCL1		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945888	chr2	181665466	181667466	NEUROD1	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	NEUROD1		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945888	chr20	20365577	20367577	INSM1	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	INSM1		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945296	chr13	31737329	31739329	Foxq1	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 	human,mouse		High+Lowthroughput	EWS-FLI1 regulates a transcriptional program in cooperation with Foxq1 in mouse Ewing sarcoma	否		Ewing sarcoma		E_02_0076	Real ‐ time quantitative PCR, luciferase assay, chip ‐ SEQ, statistical analysis	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 		In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 	Immunohistochemical staining	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 			Real‐time quantitative PCR,Luciferase assay,ChIP‐Seq,统计分析				Foxq1
29941955	chr1	186441221	186443221	PDC	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.	mouse		High+Lowthroughput	Elucidating the hypoxic stress response in barley (Hordeum vulgare L.) during waterlogging: A proteomics approach	否				E_02_0077	QRT PCR, Western blot, statistical analysis	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.		Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.	Immunohistochemical staining	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.			qRT-PCR,Western blot,统计分析				PDC
29594316	chr1	26690341	26692341	ARID1A	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	human,mouse	Lymphoid tissue, liver tissue	High+Lowthroughput	ARID1A loss in adult hepatocytes activates β-catenin-mediated erythropoietin transcription	否			erythrocyte，stem cell	E_02_0078	Immunohistochemistry and in situ hybridization experiments, enzyme-linked immunosorbent assay (ELISA), cell transfection, stimulation and luciferase assays, RNA extraction and quantitative RT-PCR, protein extracts and Western blotting, electrophoretic mobility shift assay (EMSA), flow cytometry and forming unit erythroid (CFU-E) assays, chromatin immunoprecipitation (chip) and ATAC qPCR assays were performed	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 		In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	Immunohistochemical staining	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 			免疫组化和原位杂交实验，酶联免疫吸附测定（ELISA），细胞转染、刺激和荧光素酶检测，RNA 提取和定量 RT-PCR，蛋白质提取物和蛋白质印迹，电泳迁移率移位测定 （EMSA），流式细胞术和成形单元红系 （CFU-E） 检测，染色质免疫沉淀 （ChIP） 和 ATAC-qPCR 检测				ARID1A
29593713	chr17	27054976	27056976	Nkx2-5	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	mouse	Musculature	High+Lowthroughput	Divergent Transcription of the Nkx2-5 Locus Generates Two Enhancer RNAs with Opposing Functions	否		heart failure	cardiac muscle cell (sensu Arthopoda)	E_02_0079	RNA sequencing (RNA SEQ), quantitative PCR (qPCR), cell fractionation, rna-fish, Western blotting, fluorescent immunoassay	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.		We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	Immunohistochemical staining	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.			RNA测序（RNA-seq），定量PCR（qPCR），细胞分馏，RNA-FISH，蛋白质印记，荧光免疫分析				Nkx2-5
29592873	chr13	73052423	73054423	KLF5	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	mouse	connective tissue	High+Lowthroughput	Regulation of adipocyte differentiation by clusterin-mediated Krüppel-like factor 5 stabilization	否			fat cell，mesenchymal stem cell	E_02_0080	RNA isolation and quantitative real_x0002_time PCR (qRT-PCR)，Luciferase reporter assay，20S proteasome activity assay	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.		These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	Immunohistochemical staining	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.			RNA isolation and quantitative real_x0002_time PCR (qRT-PCR)，Luciferase reporter assay，20S proteasome activity assay				KLF5
29583017	chr6	47504032	47506032	Ezh2	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	mouse	Bone marrow	High+Lowthroughput	Hematopoietic stem/progenitor cell senescence is associated with altered expression profiles of cellular memory-involved gene	否		senescence associated disease	progenitor cell	E_02_0081	qRT-PCR	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.		Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Immunohistochemical staining	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.			qRT-PCR				Ezh2
29580634	chr5	173229639	173231639	NKX2-5	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0137	Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Immunohistochemical staining	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	NKX2-5		Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.			
29579222	chr11	12671903	12673903	TEAD1	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0138	Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Immunohistochemical staining	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	TEAD1		Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease			
29579159	chr15	61854370	61856370	Myc	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	mouse	Haematopoietic tissue	High+Lowthroughput	A Myc enhancer cluster regulates normal and leukaemic haematopoietic stem cell hierarchies	否		haematopoietic malignancies	hematopoietic stem cell	E_02_0082	RT–qPCR,ATAC-seq,RNA-seq,	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies		The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	Immunohistochemical staining	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies			RT–qPCR,ATAC-seq,RNA-seq,				Myc
29576612	chr17	42310573	42312573	STAT3	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	human		High+Lowthroughput	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	否				E_01_0139	 EZH2 	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	Immunohistochemical staining	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	STAT3		 EZH2 	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity			
29572261	chr12	54030375	54032375	HOXC5	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	human	Somatic tissue	High+Lowthroughput	HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis	否		Tumor	somatic cell	E_01_0140	Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Immunohistochemical staining	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	HOXC5		Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.			
29570423	chr19	19143043	19145043	MEF2B	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	human	Lymphoid tissue	High+Lowthroughput	Comparison of Myocyte Enhancer Factor 2B Versus Other Germinal Center-associated Antigens in the Differential Diagnosis of B-Cell Non-Hodgkin Lymphomas	否		Lymphomas	B cell	E_01_0141	Immunohistochemical Staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.		Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Immunohistochemical staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.			Immunohistochemical Staining				MEF2B
29569934	chr17	43751254	43753254	SOST	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	human	Bone	High+Lowthroughput	Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis	是	rs1230399, rs7220711, rs1107748, rs75901553	osteoporosis	Germinal center B-cells	E_01_0142	Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.		The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Immunohistochemical staining	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.			Luciferase reporter assay,ChIP,qPCR				SOST
29568244	chr2	103785432	103787432	Lmo2	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	mouse	Embryo	High+Lowthroughput	BRACHYURY directs histone acetylation to target loci during mesoderm development	否		congenital diseases	hematopoietic and endothelial cell	E_02_0083	ChIP-Seq,RNA-Seq ,ChIP-qPCR	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development		T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	Immunohistochemical staining	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development			ChIP-Seq,RNA-Seq ,ChIP-qPCR				Lmo2
29564771	chr7	148804053	148806053	EZH2	EZH2 plays an important role in this inflammatory process of dental pulp.	human,mouse	dental pulp tissue	High+Lowthroughput	EZH2 regulates dental pulp inflammation by direct effect on inflammatory factors	否		dental pulp inflammation	dental pulp cell	E_02_0084	qPCR,ChIP,Western blot	EZH2 plays an important role in this inflammatory process of dental pulp.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 plays an important role in this inflammatory process of dental pulp.		EZH2 plays an important role in this inflammatory process of dental pulp.	Immunohistochemical staining	EZH2 plays an important role in this inflammatory process of dental pulp.			qPCR,ChIP,Western blot				EZH2
29563873	chr14	100892224	100894224	MEG8	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	human		High+Lowthroughput	MEG8 long noncoding RNA contributes to epigenetic progression of the epithelial-mesenchymal transition of lung and pancreatic cancer cells	否		Lung and pancreatic cancer	A549 cell，  LC-2/ad cell，Panc1 cell	E_01_0143	"Quantitative PCR，Cell migration assay，Chromatin immunoprecipitation (ChIP) assays，RNA immunoprecipitation (RIP)，Chromatin isolation by RNA purification (ChIRP) 
assays"	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."		"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	Immunohistochemical staining	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."			"Quantitative PCR，Cell migration assay，Chromatin immunoprecipitation (ChIP) assays，RNA immunoprecipitation (RIP)，Chromatin isolation by RNA purification (ChIRP) 
assays"				MEG8
29563767	chr12	55740444	55742444	GDF11	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	human		High+Lowthroughput	GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway	否		Psoriasiform skin inflammation	Mouse leukemic monocyte macrophages	E_01_0144	miRNA transfection，Real-Time PCR,Western Blot,Immunofluorescence,ELISA Assays	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	Immunohistochemical staining	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	GDF11		miRNA transfection，Real-Time PCR,Western Blot,Immunofluorescence,ELISA Assays	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 			
29563503	chr8	127077409	127079409	PRNCR1	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	human		High+Lowthroughput	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	否		Non small cell lung cancer	A549 cell, SK-MES-1 cell, Calu-3 cell，H1299 cell，NHBE cell	E_01_0145	Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 		Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Immunohistochemical staining	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 			Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay				PRNCR1
29563503	chr6	125744658	125746658	HEY2	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	human		High+Lowthroughput	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	否		Non small cell lung cancer	A549 cell, SK-MES-1 cell, Calu-3 cell，H1299 cell，NHBE cell	E_01_0145	Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Immunohistochemical staining	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	HEY2		Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 			
29563192	chr16	67559679	67561679	CTCF	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	mouse		High+Lowthroughput	Stochastic Gene Choice during Cellular Differentiation	否			embryonic stem cell	E_02_0085	Single-Cell qRT-PCR,Chromatin Immunoprecipitation,Bisulfite Sequencing	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.		The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	Immunohistochemical staining	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.			Single-Cell qRT-PCR,Chromatin Immunoprecipitation,Bisulfite Sequencing				CTCF
29563176	chr16	67559907	67561907	CTCF	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	human	blood	High+Lowthroughput	The first enhancer in an enhancer chain safeguards subsequent enhancer-promoter contacts from a distance	否			K562 cell	E_01_0146	PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Immunohistochemical staining	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	CTCF		PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.			
29563122	chr9	21074270	21076270	IFNB1	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	human	uterus	High+Lowthroughput	The Nuclear Matrix Protein SAFA Surveils Viral RNA and Facilitates Immunity by Activating Antiviral Enhancers and Super-enhancers	否			HeLa cell	E_01_0147	PCR, Western blot, flow cytometry, immunofluorescence staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Immunohistochemical staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	IFNB1		PCR,Western blot,Flow cytometry,免疫荧光染色	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).			
29563115	chr17	42310596	42312596	STAT3	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	human,mouse	connective tissue	High+Lowthroughput	Generation of Nanog reporter mice that distinguish pluripotent stem cells from unipotent primordial germ cells	否			pluripotent stem cell	E_02_0086	PCR, flow cytometry, immunofluorescence staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.		Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Immunohistochemical staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.			PCR,Flow cytometry,免疫荧光染色				STAT3
29559957	chr7	99754049	99756049	CYP3A4	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	human		High+Lowthroughput	DNA methylation determines the regulation of pregnane X receptor on CYP3A4 expression	否			HepG2 cell	E_01_0148	Plasmid construction，In vitro methylation，Luciferase reporter assay，Transfection and rifampicin induction，RNA isolation and real-time quantitative polymerase chain reaction (RT-qPCR) ，ChIP assay	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.		The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	Immunohistochemical staining	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.			Plasmid construction，In vitro methylation，Luciferase reporter assay，Transfection and rifampicin induction，RNA isolation and real-time quantitative polymerase chain reaction (RT-qPCR) ，ChIP assay				CYP3A4
29557377	chr1	156460952	156462952	MEF2D	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	human		High+Lowthroughput	A rare regulatory variant in the MEF2D gene affects gene regulation and splicing and is associated with a SLE sub-phenotype in Swedish cohorts	否			T, B, NK cell	E_01_0149	Gene array capture，Seq,Gene array capture	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 		We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	Immunohistochemical staining	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 			Gene array capture，Seq,Gene array capture				MEF2D
29556394	chr8	144311848	144313848	DGAT1	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否			mesenchymal stem cell	E_02_0087	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				DGAT1
29556394	chr10	88950906	88952906	FAS	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否			mesenchymal stem cell	E_02_0087	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				FAS
29556394	chr1	53193789	53195789	CPT2	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否			mesenchymal stem cell	E_02_0087	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				CPT2
29556082	chr11	65494664	65496664	MALAT1	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	human		High+Lowthroughput	Transcriptional Profiling of Hypoxia-Regulated Non-coding RNAs in Human Primary Endothelial Cells	否			 Primary endothelial cell	E_01_0150	GRO-Seq and RNA-Seq,	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	Immunohistochemical staining	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	MALAT1		GRO-Seq and RNA-Seq,	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 			
29554889	chr3	133743314	133745314	TF	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0151	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				TF
29554889	chr9	122199817	122201817	LHX6	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0151	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				LHX6
29554889	chr1	75125927	75127927	LHX8	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0151	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				LHX8
29552163	chr2	132413869	132415869	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse	adipose tissue	High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否		Duchenne muscular dystrophy (DMD)	satellite cell	E_02_0088	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
29552153	chr2	132413957	132415957	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse		High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否		Duchenne muscular dystrophy (DMD)	muscle cell	E_02_0089	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
29549111	chr14	21495511	21497511	METTL3	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	human		High+Lowthroughput	Disrupting the three-dimensional regulatory topology of the Pitx1 locus results in overtly normal development	否			Bone marrow stem cell	E_01_0152	flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 		The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Immunohistochemical staining	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 			flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay				METTL3
29545900	chr2	226728889	226730889	IRS1	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	human		High+Lowthroughput	Investigating a multigene prognostic assay based on significant pathways for Luminal A breast cancer through gene expression profile analysis	否			HeLa cell	E_01_0153	Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 		Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Immunohistochemical staining	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 			Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function				IRS1
29540569	chr7	148804523	148806523	EZH2	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.	mouse,	p53-dependent tissue	High+Lowthroughput	An EZH2-mediated epigenetic mechanism behind p53-dependent tissue sensitivity to DNA damage	否			Cancer cell	E_02_0090	qRT-PCR.	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.		We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.	Immunohistochemical staining	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.			qRT-PCR.				EZH2
29540468	chr17	66299977	66301977	PRKCA	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;	human		High+Lowthroughput	Genetic Reduction in Left Ventricular Protein Kinase C-α and Adverse Ventricular Remodeling in Human Subjects	是	rs9912468		non-cardiac cell	E_01_0154	PCR	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;		The PRKCA enhancer contains two common genetic variants and 4 haplotypes;	Immunohistochemical staining	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;			PCR				PRKCA
29535816	chr4	108044694	108046694	LEF1	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.	human,mouse		High+Lowthroughput	Epstein-Barr virus stably confers an invasive phenotype to epithelial cells through reprogramming of the WNT pathway	否			gastric cancer cell	E_02_0091	 RT-qPCR 	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.		The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.	Immunohistochemical staining	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.			 RT-qPCR 				LEF1
29534682	chrX	21370203	21372203	CNKSR2	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.	human,		High+Lowthroughput	Regulation of CNKSR2 protein stability by the HECT E3 ubiquitin ligase Smurf2, and its role in breast cancer progression	否				E_02_0092	RT-PCR	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.		 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.	Immunohistochemical staining	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.			RT-PCR				CNKSR2
29533787	chr2	132414173	132416173	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse		High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否			muscle cell	E_02_0093	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
29531042	chr2	42492054	42494054	MTA3	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	human,mouse	Epithelial tissues	High+Lowthroughput	Acute and Cumulative Effects of Haze Fine Particles on Mortality and the Seasonal Characteristics in Beijing, China, 2005-2013: A Time-Stratified Case-Crossover Study	否			endothelial cell	E_02_0094	PCR, Western blot, gel electrophoresis	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.		The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	Immunohistochemical staining	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.			PCR,Western blot,凝胶电泳				MTA3
29531012	chr6	36591744	36593744	SRSF3	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	human,mouse	kidney	High+Lowthroughput	The ameliorative effect of Protaetia brevitarsis Larvae in HFD-induced obese mice	否			HEK293T cell	E_02_0095	Western blot, gel electrophoresis, clip seq	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.		SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	Immunohistochemical staining	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.			Western blot,凝胶电泳,CLIP-seq				SRSF3
29530927	chr12	113389472	113391472	SDS	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	human,mouse		High+Lowthroughput	Dephosphorylation of HDAC4 by PP2A-Bδ unravels a new role for the HDAC4/MEF2 axis in myoblast fusion	否			mesenchymal stem cell	E_02_0096	PCR, Western blot, gel electrophoresis	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.		Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	Immunohistochemical staining	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.			PCR,Western blot,凝胶电泳				SDS
29530320	chr3	181709448	181711448	SOX2	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	human	lung	High+Lowthroughput	Synthetically Scalable Poly(ampholyte) Which Dramatically Enhances Cellular Cryopreservation	否			Lung squamous cell	E_01_0155	Western blot, chip SEQ, RNA SEQ, flow cytometry, gene knockdown	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	Immunohistochemical staining	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	SOX2		Western blot,ChIP-seq,RNA-seq,流式细胞术,基因敲降	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma			
29529279	chr8	94246645	94248645	GEM	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	human,mouse	liver	High+Lowthroughput	Toll-like receptor 2 stimulation augments esophageal barrier integrity	否			Huh 7 cell	E_02_0097	PCR, flow cytometry, gene knockdown, Western blot, gel electrophoresis, immunofluorescence staining	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).		In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	Immunohistochemical staining	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).			PCR,流式细胞术,基因敲降,Western blot,凝胶电泳,免疫荧光染色				GEM
29526278	chr21	33540351	33542351	SON	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).	human		High+Lowthroughput	Identification and Rescue of Splice Defects Caused by Two Neighboring Deep-Intronic ABCA4 Mutations Underlying Stargardt Disease	否				E_01_0156	RT-PCR	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).		Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).	Immunohistochemical staining	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).			RT-PCR				SON
29525407	chr7	148804989	148806989	EZH2	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].	human,mouse	 adipose tissue	High+Lowthroughput	Skeletal muscle O-GlcNAc transferase is important for muscle energy homeostasis and whole-body insulin sensitivity	否				E_02_0098	qPCR	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].		 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].	Immunohistochemical staining	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].			qPCR				EZH2
29524130	chr14	21495467	21497467	METTL3	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	human		High+Lowthroughput	Disrupting the three-dimensional regulatory topology of the Pitx1 locus results in overtly normal development	否			Bone marrow stem cell	E_01_0157	flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 		The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Immunohistochemical staining	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 			flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay				METTL3
29523836	chr2	226728284	226730284	IRS1	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	human		High+Lowthroughput	Investigating a multigene prognostic assay based on significant pathways for Luminal A breast cancer through gene expression profile analysis	否			HeLa cell	E_01_0158	Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 		Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Immunohistochemical staining	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 			Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function				IRS1
29521509	chr7	116522460	116524460	CAV1	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	mouse	lymphoid tissue	High+Lowthroughput	Rare Variant Burden Analysis within Enhancers Identifies CAV1 as an ALS Risk Gene	否			Lymphoblast	E_02_0099	Immunoblotting, fluorescent quantitative PCR (RT-PCR), immunocytochemistry, live cell imaging	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 		CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	Immunohistochemical staining	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 			免疫印迹，荧光定量 PCR（RT-PCR），免疫细胞化学，活细胞成像				CAV1
29515369	chr1	145668268	145670268	PDZK1	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	human,fish		High+Lowthroughput	A non-coding genetic variant maximally associated with serum urate levels is functionally linked to HNF4A-dependent PDZK1 expression	否	rs1967017,rs1471633	hyperuricemia	HepG2 cell	E_02_0100	Quantitative PCR, immunoblot analysis, chip PCR, statistical analysis, Weston blot	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 		 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Immunohistochemical staining	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 			Quantitative PCR,Immunoblot analysis, ChIP-PCR,统计分析,weston blot				PDZK1
29515369	chr20	44353272	44355272	HNF4A	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	human,fish		High+Lowthroughput	A non-coding genetic variant maximally associated with serum urate levels is functionally linked to HNF4A-dependent PDZK1 expression	否	rs1967017,rs1471633	hyperuricemia	HepG2 cell	E_02_0100	Quantitative PCR, immunoblot analysis, chip PCR, statistical analysis, Weston blot	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 		 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Immunohistochemical staining	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 			Quantitative PCR,Immunoblot analysis, ChIP-PCR,统计分析,weston blot				HNF4A
29514910	chr11	73215408	73217408	P2RY2	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	human,		High+Lowthroughput	Enhancer RNA - P2RY2e induced by estrogen promotes malignant behaviors of bladder cancer	否		Breast, bladder, stomach, pancreas, prostate, lung	T24 cell	E_02_0101	RT qPCR, flow cytometry, ELISA, statistical analysis	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 		P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	Immunohistochemical staining	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 			RT-qPCR,流式细胞术,ELISA,统计分析				P2RY2
29514101	chrX	67541320	67543320	AR	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 	human,mouse		High+Lowthroughput	Accelerated Evolution in Distinctive Species Reveals Candidate Elements for Clinically Relevant Traits, Including Mutation and Cancer Resistance	否				E_02_0102	DNase-seq	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 		 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 	Immunohistochemical staining	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 			DNase-seq				AR
29899112	chr6	47504499	47506499	Ezh2	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.	mouse	Nervous tissue	High+Lowthroughput	Enhancer of zeste homolog 2 (Ezh2) controls bone formation and cell cycle progression during osteogenesis in mice	否			mesenchymal stem cell of the bone marrow	E_02_0103	"RNA-Seq,Western blot,staining,RT-qPCR,MTS assays,Flow cytometric analysis,Ex vivo assays,Histology,histomorphometric analysis,Micro-computed tomography analysis,Alkaline Phosphatase and Alizarin Red
Staining,Hoechst staining,"	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.		Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.	Immunohistochemical staining	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.			"RNA-Seq,Western blot,staining,RT-qPCR,MTS assays,Flow cytometric analysis,Ex vivo assays,Histology,histomorphometric analysis,Micro-computed tomography analysis,Alkaline Phosphatase and Alizarin Red
Staining,Hoechst staining,"				Ezh2
29898989	chr3	36999364	37001216	CTCF	A CTCF-bound region within the MLH1-35 enhancer regulates MLH1 expression in colorectal cells and is worthy of scrutiny in future genetic screening strategies for suspected Lynch syndrome associated with loss of MLH1 expression.	human	Connective tissue	Low throughput	Disruption of a -35 kb Enhancer Impairs CTCF Binding and MLH1 Expression in Colorectal Cells	否	--	Lynch Syndrome		E_02_0104	ChIP-qPCR,3C,Luciferase Reporter Assay,CRISPR/Cas9	We provide the first description of an enhancer for the MLH1 gene. This -35kb enhancer was CTCF-bound, and disruption of the consensus binding site within the enhancer significantly impairs MLH1 expression in SW620 colorectal carcinoma cells.	Enhancer	3C,CRISPR/Cas9	ChIP-qPCR,Luciferase Reporter Assay	We deleted a DNA fragment corresponding to the -35kb region from SW620 cells,showed that the -35kb region functions as an MLH1 Enhancer in SW620 colorectal cells.	COCA2,FCC2,HNPCC,HNPCC2,hMLH1	--	--	--	CTCF	MRD21	CRISPR/Cas9	To evaluate the impact on endogenous MLH1 expression, we next deleted a region containing the CTCF binding motif in SW620 and K562 cells using CRISPR-Cas9 (Fig 3A, ΔCTCF). Similar to deletion of the entire Enhancer, we noted significant reduction in MLH1 expression in SW620 but not in K562 cells.	--	--	MLH1
29898989	chr3	36999364	37001216	MLH1	A CTCF-bound region within the MLH1-35 enhancer regulates MLH1 expression in colorectal cells and is worthy of scrutiny in future genetic screening strategies for suspected Lynch syndrome associated with loss of MLH1 expression.	human	Connective tissue	Low throughput	Disruption of a -35 kb Enhancer Impairs CTCF Binding and MLH1 Expression in Colorectal Cells	否	--	Lynch Syndrome		E_02_0104	ChIP-qPCR,3C,Luciferase Reporter Assay,CRISPR/Cas9	We provide the first description of an enhancer for the MLH1 gene. This -35kb enhancer was CTCF-bound, and disruption of the consensus binding site within the enhancer significantly impairs MLH1 expression in SW620 colorectal carcinoma cells.	Enhancer	3C,CRISPR/Cas9	ChIP-qPCR,Luciferase Reporter Assay	We deleted a DNA fragment corresponding to the -35kb region from SW620 cells,showed that the -35kb region functions as an MLH1 Enhancer in SW620 colorectal cells.	COCA2,FCC2,HNPCC,HNPCC2,hMLH1	--	--	--	CTCF	MRD21	CRISPR/Cas9	To evaluate the impact on endogenous MLH1 expression, we next deleted a region containing the CTCF binding motif in SW620 and K562 cells using CRISPR-Cas9 (Fig 3A, ΔCTCF). Similar to deletion of the entire Enhancer, we noted significant reduction in MLH1 expression in SW620 but not in K562 cells.	--	--	MLH1
29510148	chr14	30871809	30873809	COCH	COCH is the most abundantly expressed gene in the cochlea.	human,mouse		High+Lowthroughput	Novel loss-of-function mutations in COCH cause autosomal recessive nonsyndromic hearing loss	否			MDCK cell	E_02_0105	RT-PCR，PCR	COCH is the most abundantly expressed gene in the cochlea.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	COCH is the most abundantly expressed gene in the cochlea.		COCH is the most abundantly expressed gene in the cochlea.	Immunohistochemical staining	COCH is the most abundantly expressed gene in the cochlea.			RT-PCR，PCR				COCH
29503092	chr14	100235564	100237564	YY1	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 	human,	 adult tissue	High+Lowthroughput	YY1 Positively Regulates Transcription by Targeting Promoters and Super-Enhancers through the BAF Complex in Embryonic Stem Cells	否			pre-B cell	E_02_0106	qPCR	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 		 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 	Immunohistochemical staining	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 			qPCR				YY1
31223056	chr16	71843198	71845198	IST1	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation	human	connective tissue	High+Lowthroughput	MAPT/Tau accumulation represses autophagy flux by disrupting IST1-regulated ESCRT-III complex formation: a vicious cycle in Alzheimer neurodegeneration	否			macrophage	E_01_0159	PCR	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation		we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation	Immunohistochemical staining	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation			PCR				IST1
31221974	chr7	148804781	148806781	EZH2	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  	mouse	connective tissue	High+Lowthroughput	The Polycomb protein Ezl1 mediates H3K9 and H3K27 methylation to repress transposable elements in Paramecium	否			embryonic stem cell	E_02_0107	PCR	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  		We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  	Immunohistochemical staining	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  			PCR				EZH2
31219650	chr7	44101654	44103654	AEBP1	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 	human	Epithelial tissues	High+Lowthroughput	AEBP1, a prognostic indicator, promotes colon adenocarcinoma cell growth and metastasis through the NF-κB pathway	否			colon cancer cell	E_01_0160	PCR	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 		In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 	Immunohistochemical staining	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 			PCR				AEBP1
31219209	chr7	148805028	148807028	EZH2	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	human	connective tissue	High+Lowthroughput	Long noncoding RNA OIP5-AS1 aggravates cell proliferation, migration in gastric cancer by epigenetically silencing NLRP6 expression via binding EZH2	否		Colon cancer	gastric cancer cell	E_01_0161	PCR	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	Immunohistochemical staining	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	EZH2		PCR	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l			
31217031	chr1	26690366	26692366	ARID1A	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 	mouse	connective tissue	High+Lowthroughput	ARID1A facilitates KRAS signaling-regulated?enhancer activity in an AP1-dependent manner in colorectal cancer cells	否			tumor cell	E_02_0108	PCR	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 		We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 	Immunohistochemical staining	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 			PCR				ARID1A
31216773	chr13	27958003	27960003	CDX2	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	human	Colon tissue	High+Lowthroughput	HNF4α and CDX2 Regulate Intestinal YAP1 Promoter Activity	否			intestinal cell	E_01_0162	PCR	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	Immunohistochemical staining	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	CDX2		PCR	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.			
31216559	chr12	49973763	49975763	RACGAP1	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	human	connective tissue	High+Lowthroughput	Rac GTPase-Activating Protein 1 (RACGAP1) as an Oncogenic Enhancer in Esophageal Carcinoma	否			cancer cell	E_01_0163	PCR	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	Immunohistochemical staining	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	RACGAP1		PCR	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 			
31216030	chr19	4171371	4173371	SIRT6	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress	human	connective tissue	High+Lowthroughput	SIRT6 promotes transcription of a subset of NRF2 targets by mono-ADP-ribosylating BAF170	否			stem cell	E_01_0164	PCR	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress		SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress	Immunohistochemical staining	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress			PCR				SIRT6
31215771	chr20	56626718	56628718	TFAP2C	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	human	connective tissue	High+Lowthroughput	Comprehensive epigenetic analyses reveal master regulators driving lung metastasis of breast cancer	否		mammary cancer	breast cancer cell	E_01_0165	PCR	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	Immunohistochemical staining	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	TFAP2C		PCR	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 			
31213123	chr7	148804377	148806377	EZH2	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	human	connective tissue	High+Lowthroughput	Diosgenin exhibits tumor suppressive function via down-regulation of EZH2 in pancreatic cancer cells	否		tumour	tumor cell	E_01_0166	PCR	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	Immunohistochemical staining	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	EZH2		PCR	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.			
31205561	chr7	148804432	148806432	EZH2	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.	mouse	connective tissue	High+Lowthroughput	EZH2/Bcl-2 Coexpression Predicts Worse Survival in Diffuse Large B-cell Lymphomas and Demonstrates Poor Efficacy to Rituximab in Localized Lesions	否		tumour	tumor cell	E_02_0109	PCR	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.		Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.			PCR				EZH2
31202798	chr7	148804013	148806013	EZH2	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.	mouse	connective tissue	High+Lowthroughput	EZH2 inhibitor DZNep modulates microglial activation and protects against ischaemic brain injury after experimental stroke	否			microglial cell	E_02_0110	PCR	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.		Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.	Immunohistochemical staining	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.			PCR				EZH2
31201420	chr7	148804563	148806563	EZH2	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function	mouse	connective tissue	High+Lowthroughput	The histone methyltransferase EZH2 is required for normal uterine development and function in mice?	否			epithelial cell of uterus	E_02_0111	PCR	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function		In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function	Immunohistochemical staining	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function			PCR				EZH2
31189106	chrX	137563628	137565628	ZIC3	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation	human	connective tissue	High+Lowthroughput	ZIC3 Controls the Transition from Naive to Primed Pluripotency	否			embryonic stem cell	E_01_0167	PCR	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation		Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation	Immunohistochemical staining	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation			PCR				ZIC3
31186776	chr1	205594870	205596870	ELK4	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	human	connective tissue	High+Lowthroughput	ceRNA network analysis reveals prognostic markers for glioblastoma	否		cancer	cancer cell	E_01_0168	PCR	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	Immunohistochemical staining	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	ELK4		PCR	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.			
31186707	chr20	22578327	22580327	FOXA2	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	human	connective tissue	High+Lowthroughput	Long non-coding RNA-neighboring enhancer of FOXA2 inhibits the migration and invasion of small cell lung carcinoma cells by downregulating transforming growth factor-β1	否		lung cancer	Lung cancer cell	E_01_0169	PCR	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	Immunohistochemical staining	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	FOXA2		PCR	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T			
31182783	chr6	31161443	31163443	POU5F1	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	human	connective tissue	High+Lowthroughput	lncRNA PSORS1C3 is regulated by glucocorticoids and fine-tunes OCT4 expression in non-pluripotent cells	否			stem cell	E_01_0170	PCR	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	Immunohistochemical staining	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	POU5F1		PCR	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6			
31176714	chr18	63868870	63870870	SERPINB2	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent	mouse	connective tissue	High+Lowthroughput	Expression of Serpin Peptidase Inhibitor B2 (SERPINB2) is regulated by Aryl hydrocarbon receptor (AhR)	否		tumour	tumor cell	E_02_0112	PCR	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent		However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent	Immunohistochemical staining	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent			PCR				SERPINB2
31174563	chr11	65495199	65497199	MALAT1	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	human	connective tissue	High+Lowthroughput	Long noncoding RNA MALAT1 potentiates growth and inhibits senescence by antagonizing ABI3BP in gallbladder cancer cells	否		Gallbladder cancer	Gallbladder cancer cell	E_01_0171	PCR	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	Immunohistochemical staining	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	MALAT1		PCR	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 			
31173852	chr5	132437801	132439801	IRF1	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1	mouse	connective tissue	High+Lowthroughput	Interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma by promoting interferon response	否		ESCC	Esophageal squamous cell carcinoma cell	E_02_0113	PCR	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1		In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1	Immunohistochemical staining	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1			PCR				IRF1
31171769	chr7	148803892	148805892	EZH2	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	human	connective tissue	High+Lowthroughput	Silencing of microRNA-708 promotes cell growth and epithelial-to-mesenchymal transition by activating the SPHK2/AKT/β-catenin pathway in glioma	否		Gliomas	Glioma cell	E_01_0172	PCR	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	Immunohistochemical staining	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	EZH2		PCR	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 			
31164154	chr4	105142775	105144775	TET2	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.	mouse	connective tissue	High+Lowthroughput	Phosphorylation of TET2 by AMPK is indispensable in myogenic differentiation	否			myocyte	E_02_0114	PCR	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.		Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.	Immunohistochemical staining	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.			PCR				TET2
31164150	chr16	67559426	67561426	CTCF	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	human	epithelial cells	High+Lowthroughput	p63 cooperates with CTCF to modulate chromatin architecture in skin keratinocytes	否			glial cell	E_01_0173	PCR	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	Immunohistochemical staining	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	CTCF		PCR	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity			
31162630	chr7	148804276	148806276	EZH2	EZH2 inhibition might be a potential therapeutic target for restenosis.	human	Myotome	High+Lowthroughput	Inhibition of polycomb repressor complex 2 ameliorates neointimal hyperplasia by suppressing trimethylation of H3K27 in vascular smooth muscle cells	否			smooth muscle cell	E_01_0174	PCR	EZH2 inhibition might be a potential therapeutic target for restenosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 inhibition might be a potential therapeutic target for restenosis.	Immunohistochemical staining	EZH2 inhibition might be a potential therapeutic target for restenosis.	EZH2		PCR	EZH2 inhibition might be a potential therapeutic target for restenosis.			
31160593	chr7	148804085	148806085	EZH2	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	human	connective tissue	High+Lowthroughput	Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation	否		Colon cancer	colon cancer cell	E_01_0175	PCR	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	Immunohistochemical staining	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	EZH2		PCR	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a			
31155838	chr11	69767717	69769717	FGF4	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly	human	connective tissue	High+Lowthroughput	Critical role of the fibroblast growth factor signalling pathway in Ewing's sarcoma octamer-binding transcription factor 4-mediated cell proliferation and tumorigenesis	否		tumour	tumor cell	E_01_0176	PCR	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly		Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly	Immunohistochemical staining	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly			PCR				FGF4
31141090	chr19	33297251	33299251	CEBPA	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice	否			hematopoietic stem cell	E_02_0115	PCR	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 		Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 	Immunohistochemical staining	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 			PCR				CEBPA
31081034	chr18	55219304	55221304	TCF4	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	human	connective tissue	High+Lowthroughput	Structural basis for preferential binding of human TCF4 to DNA containing 5-carboxylcytosine	否			neural cell	E_01_0177	PCR	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	Immunohistochemical staining	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	TCF4		PCR	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.			
30995827	chr20	22578226	22580226	FOXA2	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	human	connective tissue	High+Lowthroughput	Transcriptional Regulation Factors of the Human Mitochondrial Aspartate/Glutamate Carrier Gene, Isoform 2 (SLC25A13): USF1 as Basal Factor and FOXA2 as Activator in Liver Cells	否			cancer cell	E_01_0178	PCR	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	Immunohistochemical staining	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	FOXA2		PCR	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).			
31127282	chr16	67559749	67561749	CTCF	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	human	connective tissue	High+Lowthroughput	Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping	否				E_01_0179	PCR	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	Immunohistochemical staining	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	CTCF		PCR	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).			
31064204	chr19	33297418	33299418	CEBPA	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 	mouse	connective tissue	High+Lowthroughput	Molecular cloning, characterisation, and expression patterns of pigeon CCAAT/enhancer binding protein-α and -β genes	否		cancer	cancer cell	E_02_0116	PCR	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 		In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 	Immunohistochemical staining	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 			PCR				CEBPA
31053723	chr11	2126891	2128891	IGF2	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 	human	connective tissue	High+Lowthroughput	Differential methylation of enhancer at IGF2 is associated with abnormal dopamine synthesis in major psychosis	是			neural cell	E_01_0180	PCR	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 		This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 	Immunohistochemical staining	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 			PCR				IGF2
31053176	chrX	153441659	153443659	TREX2	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 	human	connective tissue	High+Lowthroughput	DNA methylation at an enhancer of the three prime repair exonuclease 2 gene (TREX2) is linked to gene expression and survival in laryngeal cancer	是			laryngeal carcinoma cell	E_01_0181	PCR	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 		The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 	Immunohistochemical staining	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 			PCR				TREX2
31721105	chr12	117450290	117452290	KSR2	In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.	human	liver	High+Lowthroughput	Expression analysis of LTR-derived miR-1269a and target gene, KSR2 in Sebastes schlegelii	否	无	liver cancer	HCC cell	E_01_0182		In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.		In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.	Immunohistochemical staining	In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.							KSR2
31719045	chr13	63653269	63655269	Ptch1	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).	human,mouse	Musculature	High+Lowthroughput	Temporospatial sonic hedgehog signalling is essential for neural crest-dependent patterning of the intrinsic tongue musculature	否	无		muscle precursor cell	E_02_0117	PCR、Western blot	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).		We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).	Immunohistochemical staining	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).			PCR、Western blot				Ptch1
31718595	chr7	148804304	148806304	EZH2	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	human	connective tissue	High+Lowthroughput	EZH2 upregulation by ERα induces proliferation and migration of papillary thyroid carcinoma	否	无	cancer	Cancer Stem Cell	E_01_0183	PCR, Western blot, immunofluorescence staining	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	Immunohistochemical staining	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	EZH2		PCR、Western blot、免疫荧光染色	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.			
31718447	chr9	117701356	117703356	TLR4	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	human,mouse	connective tissue	High+Lowthroughput	Sphingomyelin Synthase 2 Inhibition Ameliorates Cerebral Ischemic Reperfusion Injury Through Reducing the Recruitment of Toll-Like Receptor 4 to Lipid Rafts	否	无	cerebral ischemia	B cell	E_02_0118	PCR、Western blot	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.		Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Immunohistochemical staining	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.			PCR、Western blot				TLR4
31718447	chr1	223106431	223108431	TLR5	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	human,mouse	brain	High+Lowthroughput	Sphingomyelin Synthase 2 Inhibition Ameliorates Cerebral Ischemic Reperfusion Injury Through Reducing the Recruitment of Toll-Like Receptor 5 to Lipid Rafts	否	无	cerebral ischemia	brain cell 	E_02_0118	PCR、Western blot	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.		Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Immunohistochemical staining	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.			PCR、Western blot				TLR5
31718444	chr3	43283601	43285601	SNRK	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.	human,mouse	connective tissue	High+Lowthroughput	Cardiomyocyte-Specific Snrk Prevents Inflammation in the Heart	否	无	cancer	B cell	E_02_0119	PCR、Western blot	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.		The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.	Immunohistochemical staining	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.			PCR、Western blot				SNRK
31714653	chrX	123856867	123858867	XIAP	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."	human,mouse	connective tissue	High+Lowthroughput	Apoptosis induction and ERK/NF-κB inactivation are associated with magnolol-inhibited tumor progression in hepatocellular carcinoma in vivo	否	无	liver cancer	B cell	E_02_0120	PCR	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."		"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."	Immunohistochemical staining	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."			PCR				XIAP
31713877	chr17	27753488	27755488	NOS2	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.	human,mouse	connective tissue	High+Lowthroughput	Comparative effectiveness of different antiplatelet agents at reducing TNF-driven inflammatory responses in a mouse model	否	无	Ischemic disease	immune cell	E_02_0121	PCR、Western blot	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.		Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.	Immunohistochemical staining	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.			PCR、Western blot				NOS2
31713877	chr7	150988213	150990213	NOS3	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.	human,mouse	Epithelial tissues	High+Lowthroughput	Comparative effectiveness of different antiplatelet agents at reducing TNF-driven inflammatory responses in a mouse model	否	无	Ischemic disease	blood vessel endothelial cell	E_02_0121	PCR、Western blot	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.		Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.	Immunohistochemical staining	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.			PCR、Western blot				NOS3
31712448	chr11	108808163	108810163	Axin2	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	human,mouse	Epithelial tissues	High+Lowthroughput	Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor	否	无	Cystic kidney disease	epithelial cell	E_02_0122		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Immunohistochemical staining	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells							Axin2
31712448	chr16	44910716	44912716	Ccdc80	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	human,mouse	Epithelial tissues	High+Lowthroughput	Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor	否	无	Cystic kidney disease	epithelial cell	E_02_0122		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Immunohistochemical staining	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells							Ccdc80
31712269	chr3	52218227	52220227	TLR9	pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.	human,mouse	stomach	High+Lowthroughput	Bacterial Energetic Requirements for Helicobacter pylori Cag Type IV Secretion System-Dependent Alterations in Gastric Epithelial Cells	否	无	cancer	epithelial cell of stomach	E_02_0123		pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.		pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.	Immunohistochemical staining	pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.							TLR9
31711897	chr14	54839063	54841063	GCH1	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.	mouse		High+Lowthroughput	Tetrahydrobiopterin administration facilitates amphetamine-induced dopamine release and motivation in mice	否				E_02_0124	PCR,Western blot	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.		GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.	Immunohistochemical staining	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.			PCR,Western blot				GCH1
31711520	chr7	148804473	148806473	EZH2	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].	human,mouse	connective tissue	High+Lowthroughput	HO-1 promotes resistance to an EZH2 inhibitor through the pRB-E2F pathway: correlation with the progression of myelodysplastic syndrome into acute myeloid leukemia	否		leukemia	tumor cell	E_02_0125	PCR, Western blot, immunofluorescence staining	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].		We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].	Immunohistochemical staining	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].			PCR,Western blot,免疫荧光染色				EZH2
31709534	chr1	164552565	164554565	PBX1	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.	human,mouse	connective tissue	High+Lowthroughput	Decreased levels of constitutive proteasomes in experimental autoimmune encephalomyelitis may be caused by a combination of subunit displacement and reduced Nfe2l1 expression	否		inflammation	B cell	E_02_0126	PCR, Western blot, immunofluorescence staining	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.		Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.	Immunohistochemical staining	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.			PCR,Western blot,免疫荧光染色				PBX1
31709175	chr9	127084657	127086657	ANGPTL2	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	B cell	E_02_0127	PCR,Flow cytometry	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.		Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Immunohistochemical staining	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.			PCR,Flow cytometry				ANGPTL2
31709175	chr7	22115708	22117708	RAPGEF5	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	B cell	E_02_0127	PCR,Flow cytometry	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.		Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Immunohistochemical staining	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.			PCR,Flow cytometry				RAPGEF5
31709175	chr17	35868982	35870982	CCL5	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	T cell	E_02_0127	PCR,Flow cytometry	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.		Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Immunohistochemical staining	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.			PCR,Flow cytometry				CCL5
31709175	chr5	35849791	35851791	IL7R	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	T cell	E_02_0127	PCR,Flow cytometry	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.		Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Immunohistochemical staining	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.			PCR,Flow cytometry				IL7R
31709175	chr3	39260841	39262841	CX3CR1	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	T cell	E_02_0127	PCR,Flow cytometry	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.		Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Immunohistochemical staining	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.			PCR,Flow cytometry				CX3CR1
31708105	chr5	136274432	136276432	Cux1	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	human,mouse	connective tissue	High+Lowthroughput	Cux2 expression regulated by Lhx2 in the upper layer neurons of the developing cortex	否		autism	immune cell	E_02_0128	PCR, flow cytometry, immunofluorescence staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b		Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Immunohistochemical staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b			PCR,Flow cytometry,免疫荧光染色				Cux1
31708105	chr5	121991850	121993850	Cux2	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	human,mouse	connective tissue	High+Lowthroughput	Cux2 expression regulated by Lhx2 in the upper layer neurons of the developing cortex	否		autism	immune cell	E_02_0128	PCR, flow cytometry, immunofluorescence staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b		Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Immunohistochemical staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b			PCR,Flow cytometry,免疫荧光染色				Cux2
31708105	chrX	72233135	72235135	Xlr3b	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	human,mouse	connective tissue	High+Lowthroughput	Cux2 expression regulated by Lhx2 in the upper layer neurons of the developing cortex	否		autism	immune cell	E_02_0128	PCR, flow cytometry, immunofluorescence staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b		Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Immunohistochemical staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b			PCR,Flow cytometry,免疫荧光染色				Xlr3b
31707045	chr16	56295383	56297383	Abi3bp	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Abi3bp
31707045	chr9	65169791	65171791	Cilp	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Cilp
31707045	chr9	95516985	95518985	Pcolce2	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Pcolce2
31707045	chr1	133962055	133964055	Fmod	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Fmod
31707045	chr13	49695201	49697201	Aspn	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Aspn
31707045	chr1	71621729	71623729	Fn1	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Fn1
31707045	chr17	34876882	34878882	Tnxb	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Tnxb
31707045	chr15	85088078	85090078	Fbln1	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Fbln1
31706027	chr16	67559869	67561869	CTCF	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]	human,mouse		High+Lowthroughput	Small Drosophila zinc finger C2H2 protein with an N-terminal zinc finger-associated domain demonstrates the architecture functions	否			S2 cell	E_02_0130	PCR, flow cytometry, immunofluorescence staining	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]		A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]	Immunohistochemical staining	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]			PCR,Flow cytometry,免疫荧光染色				CTCF
31705954	chr3	115620608	115622608	GAP43	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress	mouse,hippocampus	Nervous tissue	High+Lowthroughput	Fluoxetine attenuates stress-induced depressive-like behavior through modulation of hippocampal GAP43 and neurogenesis in male rats	否		depression	neural progenitor cell	E_02_0131	PCR, immunofluorescence staining	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress		The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress	Immunohistochemical staining	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress			PCR,免疫荧光染色				GAP43
31704972	chr12	55964033	55966033	CDK2	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	human,mouse		High+Lowthroughput	CDK2-mediated site-specific phosphorylation of EZH2 drives and maintains triple-negative breast cancer	否		mammary cancer	Triple-negative breast cancer cell	E_02_0132	PCR,Western blot	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).		Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Immunohistochemical staining	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).			PCR,Western blot				CDK2
31704972	chr7	148804376	148806376	EZH2	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	human,mouse	breast	High+Lowthroughput	CDK2-mediated site-specific phosphorylation of EZH2 drives and maintains triple-negative breast cancer	否		mammary cancer	mammary gland epithelial cell	E_02_0132	PCR,Western blot	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).		Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Immunohistochemical staining	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).			PCR,Western blot				EZH2
31699991	chr17	42697602	42699602	EZH1	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 	human,mouse	connective tissue	High+Lowthroughput	Protein lysine 43 methylation by EZH1 promotes AML1-ETO transcriptional repression in leukemia	否		cancer	stem cell	E_02_0133	PCR,Western blot	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 		Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 	Immunohistochemical staining	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 			PCR,Western blot				EZH1
31698854	chrX	25000875	25002875	ARX	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				ARX
31698854	chr12	121623759	121625759	ORAI1	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				ORAI1
31698854	chrX	159552038	159554038	Cdkl5	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				Cdkl5
31698854	chr3	55147134	55149134	Dclk1	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				Dclk1
31698100	chr20	13993019	13995019	MACROD2	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	human		High+Lowthroughput	Split hand/foot malformation associated with 20p12.1 deletion: A case report	是		Split hand / foot malformation		E_01_0184	PCR	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 		Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Immunohistochemical staining	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 			PCR				MACROD2
31698100	chr20	16269065	16271065	KIF16B	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	human		High+Lowthroughput	Split hand/foot malformation associated with 20p12.1 deletion: A case report	是		Split hand / foot malformation		E_01_0184	PCR	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 		Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Immunohistochemical staining	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 			PCR				KIF16B
31697837	chr5	88714150	88716150	MEF2C	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.	human,mouse	connective tissue	High+Lowthroughput	Salt-inducible kinase inhibition suppresses acute myeloid leukemia progression in vivo	否		Acute myeloid leukemia	mutant lymphoma cell	E_02_0135	PCR,Flow cytometry,Western blot	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.		In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.	Immunohistochemical staining	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.			PCR,Flow cytometry,Western blot				MEF2C
31695501	chr7	148804320	148806320	EZH2	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.	human,mouse	connective tissue	High+Lowthroughput	Silencing Of hsa_circ_0008450 Represses Hepatocellular Carcinoma Progression Through Regulation Of microRNA-214-3p/EZH2 Axis	否		liver cancer	cancer cell	E_02_0136	PCR,Western blot	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.		Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.	Immunohistochemical staining	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.			PCR,Western blot				EZH2
31695196	chr17	40016366	40018366	MED24	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.	human,mouse	connective tissue	High+Lowthroughput	Silencing Of hsa_circ_0008450 Represses Hepatocellular Carcinoma Progression Through Regulation Of microRNA-214-3p/EZH2 Axis	否	无		embryonic stem cell	E_02_0137	PCR,Flow cytometry	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.		ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.	Immunohistochemical staining	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.			PCR,Flow cytometry				MED24
31694243	chr4	186066778	186068778	TLR3	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.	human,mouse	blood	High+Lowthroughput	Transcriptome analysis reveals a positive effect of brassinosteroids on the photosynthetic capacity of wucai under low temperature	否	无	leukemia	B cell	E_02_0138	PCR,Western blot	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.		Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.	Immunohistochemical staining	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.			PCR,Western blot				TLR3
31694013	chr7	148804620	148806620	EZH2	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	human	intestines	High+Lowthroughput	Oleanolic Acid Acetate Exerts Anti-Inflammatory Activity via IKKα/β Suppression in TLR3-Mediated NF-κB Activation	否	无	Colon cancer	colon cancer cell	E_01_0185	PCR	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	EZH2		PCR	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities			
31693890	chr7	148804304	148806304	EZH2	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	human	breast	High+Lowthroughput	Enhancer of Zeste Homolog 2 in Colorectal Cancer Development and Progression	否	无	mammary cancer	breast cancer cell	E_01_0186	PCR,Western blot,Flow cytometry	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	Immunohistochemical staining	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	EZH2		PCR,Western blot,Flow cytometry	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.			
31693439	chr15	90963083	90965083	PRC1	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1	human	bone marrow	High+Lowthroughput	Regulation of EZH2 by SMYD2-Mediated Lysine Methylation Is Implicated in Tumorigenesis	否	无	Myeloma	Myeloma cell	E_01_0187	PCR,Western blot,Flow cytometry	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1		Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1	Immunohistochemical staining	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1			PCR,Western blot,Flow cytometry				PRC1
31692936	chr4	1868930	1870930	NSD2	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance	human,mouse	kidney	High+Lowthroughput	Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments	否	无	renal cell carcinoma	Renal cell	E_02_0139	PCR,Western blot,Flow cytometry	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance		NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance	Immunohistochemical staining	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance			PCR,Western blot,Flow cytometry				NSD2
31692093	chr17	82215342	82217342	SLC16A3	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.	human,mouse	intervertebral disc	High+Lowthroughput	Combining GAL4 GFP enhancer trap with split luciferase to measure spatiotemporal promoter activity in Arabidopsis	否	无	Chronic intervertebral pain	intervertebral disc cells	E_02_0140	PCR, Western blot, flow cytometry, immunofluorescence staining	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.		Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.	Immunohistochemical staining	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.			PCR,Western blot,Flow cytometry,免疫荧光染色				SLC16A3
31692040	chr12	55964023	55966023	CDK2	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells	human,mouse	bone marrow	High+Lowthroughput	Lactate Efflux From Intervertebral Disc Cells Is Required for Maintenance of Spine Health	否	无	Myeloid leukemia	myeloid leukemia cells	E_02_0141	PCR, Western blot, flow cytometry, immunofluorescence staining	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells		In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells	Immunohistochemical staining	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells			PCR,Western blot,Flow cytometry,免疫荧光染色				CDK2
31692040	chr19	33297357	33299357	CEBPA	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.	human,mouse	liver	High+Lowthroughput	Lactate Efflux From Intervertebral Disc Cells Is Required for Maintenance of Spine Health	否	无	tumour	hepatocyte	E_02_0141	PCR, Western blot, flow cytometry, immunofluorescence staining	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.		Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.	Immunohistochemical staining	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.			PCR,Western blot,Flow cytometry,免疫荧光染色				CEBPA
31691800	chr21	39443054	39445054	SH3BGR	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.	human,mouse	Epithelial tissues	High+Lowthroughput	Berberine Inhibits Adipogenesis in Porcine Adipocytes via AMP-Activated Protein Kinase-Dependent and -Independent Mechanisms	是	rs2836411	Abdominal aortic aneurysm	blood vessel endothelial cell	E_02_0142	PCR,Flow cytometry	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.		Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.	Immunohistochemical staining	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.			PCR,Flow cytometry				SH3BGR
31690584	chr17	72118178	72120178	SOX9	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	human	breast	High+Lowthroughput	The hTERT-VNTR2-2(nd) alleles are involved in genomic stability in gastrointestinal cancer	否	无	mammary cancer	breast cancer cell	E_01_0188	PCR, Western blot, gene knockdown	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	Immunohistochemical staining	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	SOX9		PCR,Western blot,基因敲降	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase			
31689455	chr7	100717697	100719697	EPO	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.	human,mouse	Musculature	High+Lowthroughput	Erythropoietin attenuates vascular calcification by inhibiting endoplasmic reticulum stress in rats with chronic kidney disease	否	无	Vascular calcification	smooth muscle cell	E_02_0143	Western blot,PCR	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.		EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.	Immunohistochemical staining	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.			Western blot,PCR				EPO
31689455	chr19	11374596	11376596	EPOR	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells	human,mouse	connective tissue	High+Lowthroughput	Erythropoietin attenuates vascular calcification by inhibiting endoplasmic reticulum stress in rats with chronic kidney disease	否	无	Vascular calcification	target cell	E_02_0143	Western blot,PCR	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells		The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells	Immunohistochemical staining	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells			Western blot,PCR				EPOR
31686316	chr22	39516753	39518753	ATF4	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells	否	无	atherosclerosis	macrophage derived foam cell	E_02_0144	Western blot,PCR	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.		We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Immunohistochemical staining	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.			Western blot,PCR				ATF4
31686316	chr1	161763620	161765620	ATF6	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells	否	无	atherosclerosis	macrophage derived foam cell	E_02_0144	Western blot,PCR	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.		We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Immunohistochemical staining	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.			Western blot,PCR				ATF6
31686316	chr6	106042776	106044776	ATG5	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells	否	无	atherosclerosis	immune cell	E_02_0144	Western blot,PCR	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.		We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Immunohistochemical staining	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.			Western blot,PCR				ATG5
31686214	chr16	86507862	86509862	FOXF1	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.	human,mouse	Epithelial tissues	High+Lowthroughput	Association of rare non-coding SNVs in the lung-specific FOXF1 enhancer with a mitigation of the lethal ACDMPV phenotype	是	rs150502618-A	Misalignment of pulmonary veins	epithelial cell	E_02_0145	Flow cytometry,PCR	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.		Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.	Immunohistochemical staining	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.			Flow cytometry,PCR				FOXF1
31686214	chr16	67559674	67561674	CTCF	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 	human,mouse	lung	High+Lowthroughput	Association of rare non-coding SNVs in the lung-specific FOXF1 enhancer with a mitigation of the lethal ACDMPV phenotype	是	rs79301423-T	Misalignment of pulmonary veins	pneumocyte	E_02_0145	Flow cytometry,PCR	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 		Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 	Immunohistochemical staining	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 			Flow cytometry,PCR				CTCF
31684161	chr4	153681439	153683439	TLR2	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	human,mouse	blood	High+Lowthroughput	HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule	否	无	inflammation	B cell	E_02_0146	Western blot,PCR	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 		The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Immunohistochemical staining	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 			Western blot,PCR				TLR2
31684161	chr9	117701075	117703075	TLR4	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	human,mouse	connective tissue	High+Lowthroughput	HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule	否	无	inflammation	immune cell	E_02_0146	Western blot,PCR	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 		The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Immunohistochemical staining	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 			Western blot,PCR				TLR4
31682213	chr20	44582166	44584166	ADA	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).	human	connective tissue	High+Lowthroughput	An Assessment of the Effects of Azodicarbonamide-containing Diet on Neurobehaviour, Brain Antioxidant Status and Membrane Lipid Peroxidation Status in Rats	否	无			E_01_0189	PCR	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).		Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).	Immunohistochemical staining	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).			PCR				ADA
31681405	chr14	100235887	100237887	YY1	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.	human,mouse		High+Lowthroughput	Enhancer LncRNAs Influence Chromatin Interactions in Different Ways	是	无		GM12878 cell	E_02_0147	Flow cytometry	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.		The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.	Immunohistochemical staining	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.			Flow cytometry				YY1
31681009	chr8	19899234	19901234	LPL	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages	human,mouse	connective tissue	High+Lowthroughput	Ghrelin Promotes Proliferation and Inhibits Differentiation of 3T3-L1 and Human Primary Preadipocytes	否	无		pluripotent stem cell	E_02_0148	Western blot,PCR	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages		For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages	Immunohistochemical staining	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages			Western blot,PCR				LPL
31680128	chr11	1155000	1157000	MUC5AC	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases	human	Epithelial tissues	High+Lowthroughput	Fipronil upregulates inflammatory cytokines and MUC5AC expression in human nasal epithelial cells	否	无	airway inflammation 	epithelial cell	E_01_0190	Western blot,PCR	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases		 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases	Immunohistochemical staining	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases			Western blot,PCR				MUC5AC
31679819	chr12	48826675	48828675	DDX23	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.	human,mouse	uterus	High+Lowthroughput	R-Loops Promote Antisense Transcription across the Mammalian Genome	否	无		HeLa cell	E_02_0149	Western blot,PCR,Flow cytometry	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.		Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.	Immunohistochemical staining	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.			Western blot,PCR,Flow cytometry				DDX23
31679819	chr2	144361373	144363373	ZEB2	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.	human,mouse	connective tissue	High+Lowthroughput	R-Loops Promote Antisense Transcription across the Mammalian Genome	否	无		stem cell	E_02_0149	Western blot,PCR,Flow cytometry	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.		Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.	Immunohistochemical staining	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.			Western blot,PCR,Flow cytometry				ZEB2
31678303	chr1	156461181	156463181	MEF2D	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 	human,mouse	liver	High+Lowthroughput	Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells	否	无	liver cancer	hepatocellular carcinoma cell	E_02_0150	Western blot, PCR, flow cytometry, immunofluorescence staining	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 		MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 	Immunohistochemical staining	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 			Western blot,PCR,Flow cytometry,免疫荧光染色				MEF2D
31678303	chr17	81909215	81911215	SIRT7	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.	human,mouse	blood	High+Lowthroughput	Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells	否	无	liver cancer	T cell	E_02_0150	Western blot, PCR, flow cytometry, immunofluorescence staining	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.		Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.	Immunohistochemical staining	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.			Western blot,PCR,Flow cytometry,免疫荧光染色				SIRT7
31678303	chr9	5447414	5449414	CD274	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 	human,mouse	connective tissue	High+Lowthroughput	Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells	否	无	liver cancer	immune cell	E_02_0150	Western blot, PCR, flow cytometry, immunofluorescence staining	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 		MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 	Immunohistochemical staining	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 			Western blot,PCR,Flow cytometry,免疫荧光染色				CD274
31676868	chr20	40683274	40685274	MAFB	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	human	blood	High+Lowthroughput	The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes	是	rs78037977	diabetes	B cell	E_01_0191	Flow cytometry,PCR	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	Immunohistochemical staining	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	MAFB		Flow cytometry,PCR	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.			
31676868	chr16	11251612	11253612	SOCS1	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	human	connective tissue	High+Lowthroughput	The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes	是	rs193778	diabetes	EC cell	E_01_0191	Flow cytometry,PCR	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Immunohistochemical staining	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	SOCS1		Flow cytometry,PCR	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.			
31676868	chr16	10925964	10927964	DEXI	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	human	connective tissue	High+Lowthroughput	The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes	是	rs193778	diabetes	EC cell	E_01_0191	Flow cytometry,PCR	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.		The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Immunohistochemical staining	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.			Flow cytometry,PCR				DEXI
31676828	chr1	92469783	92471783	GFI1	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 	human,mouse	blood	High+Lowthroughput	LSD1-mediated repression of GFI1 super-enhancer plays an essential role in erythroleukemia	否	无	leukemia	leukemic cell	E_02_0151	Flow cytometry,PCR	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 		In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 	Immunohistochemical staining	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 			Flow cytometry,PCR				GFI1
31676673	chrX	49025404	49027404	TFE3	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.	human,mouse	blood	High+Lowthroughput	Folliculin Interacting Protein 1 Maintains Metabolic Homeostasis during B Cell Development by Modulating AMPK, mTORC1, and TFE3	否	无		B cell	E_02_0152	Flow cytometry,PCR	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.		Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.	Immunohistochemical staining	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.			Flow cytometry,PCR				TFE3
31675590	chr7	148804429	148806429	EZH2	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.	human,mouse	connective tissue	High+Lowthroughput	The carcinogen cadmium elevates CpG-demethylation and enrichment of NFYA and E2F1 in the promoter of oncogenic PRMT5 and EZH2 methyltransferases resulting in their elevated expression in?vitro	否	无	cancer	HepG2 cell	E_02_0153	Western blot,PCR,Flow cytometry	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.		Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.	Immunohistochemical staining	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.			Western blot,PCR,Flow cytometry				EZH2
31672165	chr17	47197711	47199711	MYL4	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.	mouse	blood	High+Lowthroughput	Contaminating reactivity of a monoclonal CCAAT/Enhancer Binding Protein β antibody in differentiating myoblasts	否	无		B cell	E_02_0154	Western blot	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.		Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.	Immunohistochemical staining	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.			Western blot				MYL4
31668620	chr13	118804154	118806154	Fgf10	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 	mouse	Musculature	High+Lowthroughput	Attenuated Fgf Signaling Underlies the Forelimb Heterochrony in the Emu Dromaius novaehollandiae	否	无		muscle cell	E_02_0155	Flow cytometry, PCR, immunofluorescence staining	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 		Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 	Immunohistochemical staining	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 			Flow cytometry,PCR,免疫荧光染色				Fgf10
31666694	chr11	69983276	69985276	ANO1	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	human	Stomach, gut	High+Lowthroughput	Altered chromosomal topology drives oncogenic programs in SDH-deficient GISTs	否	无	Gastrointestinal stromal tumors	GIST-T1 cell	E_01_0192	Flow cytometry	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	Immunohistochemical staining	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	ANO1		Flow cytometry	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).			
31666665	chr7	148804251	148806251	EZH2	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9	human,mouse	lung	High+Lowthroughput	Cigarette smoke affects the onco-suppressor DAB2IP expression in bronchial epithelial cells of COPD patients	否	无	lung cancer	Lung cancer cell	E_02_0156	PCR, Western blot, immunofluorescence staining	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9		Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9	Immunohistochemical staining	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9			PCR,Western blot,免疫荧光染色				EZH2
31666509	chr3	38545360	38547360	SCN5A	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.	human,mouse	heart	High+Lowthroughput	An enhancer cluster controls gene activity and topology of the SCN5A-SCN10A locus in vivo	是	rs6810361	Arrhythmia	cardiac muscle cell (sensu Arthopoda)	E_02_0157	Flow cytometry,PCR	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.		Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.	Immunohistochemical staining	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.			Flow cytometry,PCR				SCN5A
31666509	chr3	38694445	38696445	SCN10A	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.	human,mouse	connective tissue	High+Lowthroughput	An enhancer cluster controls gene activity and topology of the SCN5A-SCN10A locus in vivo	是	rs6781009	Arrhythmia	embryonic stem cell	E_02_0157	Flow cytometry,PCR	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.		The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.	Immunohistochemical staining	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.			Flow cytometry,PCR				SCN10A
31666072	chr17	50181276	50183276	COL1A1	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	human	Epithelial tissues	High+Lowthroughput	Epigenetic landscapes suggest that genetic risk for intracranial aneurysm operates on the endothelium	是	rs1333040	inflammation	endothelial cell	E_01_0193	ChIP-Seq	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	Immunohistochemical staining	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	COL1A1		ChIP-Seq	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].			
31665646	chrX	73818246	73820246	XIST	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "	human,mouse	connective tissue	High+Lowthroughput	Mapping Native R-Loops Genome-wide Using a Targeted Nuclease Approach	否	无	cancer	HEK293 cell	E_02_0158	Flow cytometry,PCR	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "		"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "	Immunohistochemical staining	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "			Flow cytometry,PCR				XIST
31665330	chr16	68733997	68735997	CDH1	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	human,mouse	Epithelial tissues	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	epithelial cell	E_02_0159	PCR	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 		On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Immunohistochemical staining	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 			PCR				CDH1
31665330	chr13	73052330	73054330	KLF5	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	human,mouse	Epithelial tissues	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	epithelial cell	E_02_0159	PCR	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 		On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Immunohistochemical staining	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 			PCR				KLF5
31665330	chr16	28529423	28531423	NUPR1	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	mouse	blood	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	B cell	E_02_0159	PCR	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.		Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Immunohistochemical staining	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.			PCR				NUPR1
31665330	chr12	131947347	131949347	EP400	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	mouse	blood	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	B cell	E_02_0159	PCR	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.		Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Immunohistochemical staining	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.			PCR				EP400
31665135	chr8	116842944	116844944	RAD21	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	human,mouse	blood	High+Lowthroughput	EAGLE: An algorithm that utilizes a small number of genomic features to predict tissue/cell type-specific enhancer-gene interactions	否	无			E_02_0160	Flow cytometry,PCR	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.		Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Immunohistochemical staining	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.			Flow cytometry,PCR				RAD21
31665135	chr16	67559548	67561548	CTCF	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	human,mouse	uterus	High+Lowthroughput	EAGLE: An algorithm that utilizes a small number of genomic features to predict tissue/cell type-specific enhancer-gene interactions	否	无		Hela-S3 cell	E_02_0160	Flow cytometry,PCR	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.		Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Immunohistochemical staining	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.			Flow cytometry,PCR				CTCF
31665067	chr18	55219450	55221450	TCF4	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	human	bone	High+Lowthroughput	CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to enhance the transcriptional activity of β-catenin/LEF1 complex via effects on chromatin remodeling	否	无	Osteosarcoma	osteosarcoma cell	E_01_0194	Flow cytometry,PCR,Western blot	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	Immunohistochemical staining	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	TCF4		Flow cytometry,PCR,Western blot	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].			
31665067	chr5	16658965	16660965	MYO10	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].	human	connective tissue	High+Lowthroughput	CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to enhance the transcriptional activity of β-catenin/LEF1 complex via effects on chromatin remodeling	否	无	Osteosarcoma	mesenchymal stem cell	E_01_0194	Flow cytometry,PCR,Western blot	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].		In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].	Immunohistochemical staining	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].			Flow cytometry,PCR,Western blot				MYO10
31664109	chrX	154007840	154009840	IRAK1	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	human	blood	High+Lowthroughput	IRAK3 modulates downstream innate immune signalling through its guanylate cyclase activity	是	无	inflammation	B cell	E_01_0195	PCR	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 		IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Immunohistochemical staining	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 			PCR				IRAK1
31664109	chr12	43756484	43758484	IRAK4	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	human	blood	High+Lowthroughput	IRAK3 modulates downstream innate immune signalling through its guanylate cyclase activity	是	无	inflammation	B cell	E_01_0195	PCR	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 		IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Immunohistochemical staining	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 			PCR				IRAK4
31662342	chr16	86508235	86510235	FOXF1	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).	human,mouse	Epithelial tissues	High+Lowthroughput	Disruption of normal patterns of FOXF1 expression in a lethal disorder of lung development	否	无	cancer	endothelial cell	E_02_0161	Flow cytometry,PCR,Western blot	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).		Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).	Immunohistochemical staining	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).			Flow cytometry,PCR,Western blot				FOXF1
31661141	chr12	2855382	2857382	FOXM1	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	human,mouse	uterus	High+Lowthroughput	Crosstalk between histone modification and DNA methylation orchestrates the epigenetic regulation of the costimulatory factors, Tim?3 and galectin?9, in cervical cancer	否	无	cervical carcinoma	HeLa cell	E_02_0162	PCR,Western blot	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).		In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Immunohistochemical staining	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).			PCR,Western blot				FOXM1
31661141	chr7	148804354	148806354	EZH2	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	human,mouse	blood	High+Lowthroughput	Crosstalk between histone modification and DNA methylation orchestrates the epigenetic regulation of the costimulatory factors, Tim?3 and galectin?9, in cervical cancer	否	无	cervical carcinoma	T cell	E_02_0162	PCR,Western blot	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).		In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Immunohistochemical staining	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).			PCR,Western blot				EZH2
31661121	chr17	58267209	58269209	MPO	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 	human,mouse	Epithelial tissues	High+Lowthroughput	Dihydroartemisinin attenuates lipopolysaccharide?induced acute lung injury in mice by suppressing NF?κB signaling in an Nrf2?dependent manner	否	无	inflammation	epithelial cell	E_02_0163	PCR, Western blot, immunofluorescence staining	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 		Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 	Immunohistochemical staining	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 			PCR,Western blot,免疫荧光染色				MPO
31659808	chr2	237482764	237484764	MLPH	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.	human	prostate	High+Lowthroughput	Single-nucleotide polymorphism rs13426236 contributes to an increased prostate cancer risk via regulating MLPH splicing variant 4	是	rs13426236	prostatic cancer	prostate cancer cell	E_01_0196	Flow cytometry,Western blot,PCR	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.		To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.	Immunohistochemical staining	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.			Flow cytometry,Western blot,PCR				MLPH
31659207	chr11	128455802	128457802	ETS1	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	human	blood	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs9888739	Systemic lupus erythematosus	T cell	E_01_0197	Flow cytometry,PCR	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	Immunohistochemical staining	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	ETS1		Flow cytometry,PCR	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.			
31659207	chrX	49247778	49249778	FOXP3	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	human	connective tissue	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs1143679	Systemic lupus erythematosus	stem cell	E_01_0197	Flow cytometry,PCR	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	Immunohistochemical staining	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	FOXP3		Flow cytometry,PCR	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).			
31659207	chr5	151027114	151029114	TNIP1	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	human	blood	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs10488631	Systemic lupus erythematosus	B cell	E_01_0197	Flow cytometry,PCR	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	Immunohistochemical staining	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	TNIP1		Flow cytometry,PCR	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).			
31659207	chr7	128934736	128936736	IRF5	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	human	connective tissue	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs4728142	Systemic lupus erythematosus	B-lymphoblastoid cells	E_01_0197	Flow cytometry,PCR	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	Immunohistochemical staining	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	IRF5		Flow cytometry,PCR	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.			
31659207	chrX	12864199	12866199	TLR7	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.	human	connective tissue	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs1128334	Systemic lupus erythematosus	immune cell	E_01_0197	Flow cytometry,PCR	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.		Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.	Immunohistochemical staining	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.			Flow cytometry,PCR				TLR7
31659207	chr7	128951769	128953769	TNPO3	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.	human	blood	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs6590330	Systemic lupus erythematosus		E_01_0197	Flow cytometry,PCR	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.		The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.	Immunohistochemical staining	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.			Flow cytometry,PCR				TNPO3
31659164	chr8	11673920	11675920	GATA4	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	human	connective tissue	High+Lowthroughput	A reference map of murine cardiac transcription factor chromatin occupancy identifies dynamic and conserved enhancers	否	无	cancer	stem cell	E_01_0198	PCR,Flow cytometry	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	Immunohistochemical staining	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	GATA4		PCR,Flow cytometry	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 			
31659164	chr5	173229614	173231614	NKX2-5	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	human	Musculature	High+Lowthroughput	A reference map of murine cardiac transcription factor chromatin occupancy identifies dynamic and conserved enhancers	否	无	cancer	muscle cell	E_01_0198	PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Immunohistochemical staining	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	NKX2-5		PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 			
31659164	chr15	99562305	99564305	MEF2A	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	human	Musculature	High+Lowthroughput	A reference map of murine cardiac transcription factor chromatin occupancy identifies dynamic and conserved enhancers	否	无	cancer	muscle cell	E_01_0198	PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Immunohistochemical staining	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	MEF2A		PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 			
31659118	chr7	97849158	97851158	ASNS	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "	human,mouse	tumour	High+Lowthroughput	Promoter demethylation of the asparagine synthetase gene is required for ATF4-dependent adaptation to asparagine depletion	否	无	acute lymphoblastic leukemia	tumor cell	E_02_0164	Flow cytometry,Western blot,PCR	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "		"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "	Immunohistochemical staining	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "			Flow cytometry,Western blot,PCR				ASNS
31659118	chr1	28257099	28259099	SESN2	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).	human,mouse	blood	High+Lowthroughput	Promoter demethylation of the asparagine synthetase gene is required for ATF4-dependent adaptation to asparagine depletion	否	无	acute lymphoblastic leukemia	Nalm-6 cell	E_02_0164	Flow cytometry,Western blot,PCR	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).		As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).	Immunohistochemical staining	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).			Flow cytometry,Western blot,PCR				SESN2
31658410	chr14	48891897	48893897	Otx2	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.	human,mouse	connective tissue	High+Lowthroughput	A distal enhancer that directs Otx2 expression in the retinal pigment epithelium and neuroretina	否	无		pluripotent stem cell	E_02_0165	Flow cytometry, immunofluorescence staining	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.		Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.	Immunohistochemical staining	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.			Flow cytometry，免疫荧光染色				Otx2
31658410	chr11	31781903	31783903	PAX6	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation	human,mouse	Nervous tissue	High+Lowthroughput	A distal enhancer that directs Otx2 expression in the retinal pigment epithelium and neuroretina	否	无		photoreceptor cell	E_02_0165	Flow cytometry, immunofluorescence staining	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation		In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation	Immunohistochemical staining	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation			Flow cytometry，免疫荧光染色				PAX6
31657619	chr1	26690155	26692155	ARID1A	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	human,mouse	connective tissue	High+Lowthroughput	Altered 5-Hydroxymethylcytosine Landscape in Primary Gastric Adenocarcinoma	否	无	gastric cancer	embryonic stem cell	E_02_0166	PCR	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"		"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Immunohistochemical staining	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"			PCR				ARID1A
31657619	chr10	121475438	121477438	FGFR2	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	human,mouse	connective tissue	High+Lowthroughput	Altered 5-Hydroxymethylcytosine Landscape in Primary Gastric Adenocarcinoma	否	无	gastric cancer	embryonic stem cell	E_02_0166	PCR	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"		"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Immunohistochemical staining	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"			PCR				FGFR2
31654083	chr17	44073800	44075800	HDAC5	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "	human,mouse	blood	High+Lowthroughput	Early-life blockade of NMDA receptors induces epigenetic abnormalities in the adult medial prefrontal cortex: possible involvement in memory impairment in trace fear conditioning	否	无	Schizophrenia		E_02_0167	PCR,Western blot 	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "		"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "	Immunohistochemical staining	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "			PCR,Western blot 				HDAC5
31653691	chr12	107873350	107875350	Bcl11b	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.	human,mouse	blood	High+Lowthroughput	Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells	否	无		mutant lymphoma cell	E_02_0168	Flow cytometry,Western blot,PCR	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.		To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.	Immunohistochemical staining	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.			Flow cytometry,Western blot,PCR				Bcl11b
31653691	chr16	92395674	92397674	Runx1	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.	human,mouse	lymph	High+Lowthroughput	Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells	否	无		lymphocyte	E_02_0168	Flow cytometry,Western blot,PCR	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.		Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.	Immunohistochemical staining	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.			Flow cytometry,Western blot,PCR				Runx1
31653691	chr10	8042938	8044938	GATA3	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3	human,mouse	blood	High+Lowthroughput	Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells	否	无		T cell	E_02_0168	Flow cytometry,Western blot,PCR	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3		These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3	Immunohistochemical staining	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3			Flow cytometry,Western blot,PCR				GATA3
31652979	chr8	127732500	127734500	MYC	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.	human,mouse	breast	High+Lowthroughput	PIK3CA Cooperates with KRAS to Promote MYC Activity and Tumorigenesis via the Bromodomain Protein BRD9	否	无	tumour	mammary gland epithelial cell	E_02_0169	Western blot	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.		Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.	Immunohistochemical staining	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.			Western blot				MYC
31652453	chr7	148804156	148806156	EZH2	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	human	bone	High+Lowthroughput	Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix	否	无	Osteosarcoma	osteosarcoma cell	E_01_0199	Flow cytometry, Western blot, PCR, immunofluorescence light staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Immunohistochemical staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	EZH2		Flow cytometry,Western blot,PCR,免疫荧光光染色	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23			
31652453	chr9	94600340	94602340	FBP1	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	human	bone	High+Lowthroughput	Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix	否	无	Osteosarcoma	osteosarcoma cell	E_01_0199	Flow cytometry, Western blot, PCR, immunofluorescence light staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23		FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Immunohistochemical staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23			Flow cytometry,Western blot,PCR,免疫荧光光染色				FBP1
31651209	chr2	236162410	236164410	GBX2	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	human,mouse		High+Lowthroughput	GSK343 induces programmed cell death through the inhibition of EZH2 and FBP1 in osteosarcoma cells	否	无	Nerve injury	Schwann cell	E_02_0170	PCR, Western blot, immunofluorescence staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.		A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Immunohistochemical staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.			PCR,Western blot ,免疫荧光染色				GBX2
31651209	chr11	114056802	114058802	ZBTB16	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	human,mouse		High+Lowthroughput	GSK343 induces programmed cell death through the inhibition of EZH2 and FBP1 in osteosarcoma cells	否	无	Nerve injury	Schwann cell	E_02_0170	PCR, Western blot, immunofluorescence staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.		A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Immunohistochemical staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.			PCR,Western blot ,免疫荧光染色				ZBTB16
31650361	chr2	236162780	236164780	GBX2	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -	human,mouse	connective tissue	High+Lowthroughput	Dysregulated Transcription Factor TFAP2A After Peripheral Nerve Injury Modulated Schwann Cell Phenotype	否	无		Schwann cell	E_02_0171	Western blot, PCR, gene knockdown	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -		A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -	Immunohistochemical staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -			Western blot,PCR,基因敲降				GBX2
31649847	chr11	70018598	70020598	Mgl2	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).	human,mouse	connective tissue	High+Lowthroughput	Kinsenoside attenuates osteoarthritis by repolarizing macrophages through inactivating NF-κB/MAPK signaling and protecting chondrocytes	否	无	Osteoarthritis	macrophage	E_02_0172	PCR, Western blot, flow cytometry, gene knockdown	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).		Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).	Immunohistochemical staining	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).			PCR,Western blot,Flow cytometry,基因敲降				Mgl2
31649059	chr1	8001795	8003795	ERRFI1	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "	human	blood	High+Lowthroughput	Identification and dynamic quantification of regulatory elements using total RNA	否	无	leukemia	myelogenous leukemia cell	E_01_0200	Flow cytometry	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "		"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "	Immunohistochemical staining	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "			Flow cytometry				ERRFI1
31649055	chr2	47342302	47344302	EPCAM	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	human	connective tissue	High+Lowthroughput	FFPEcap-seq: a method for sequencing capped RNAs in formalin-fixed paraffin-embedded samples	是	无	leukemia	stromal macrophage cell	E_01_0201	Flow cytometry	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	Immunohistochemical staining	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	EPCAM		Flow cytometry	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "			
31649032	chr3	66876146	66878146	Shox2	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 	human	connective tissue	High+Lowthroughput	Shox2 regulates osteogenic differentiation and pattern formation during hard palate development in mice	否	无		mesenchymal cell	E_01_0202	Flow cytometry, PCR, immunofluorescence staining	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 		Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 	Immunohistochemical staining	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 			Flow cytometry,PCR,免疫荧光染色				Shox2
31644911	chr8	101489945	101491945	GRHL2	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).	human,mouse	breast	High+Lowthroughput	The Lineage Determining Factor GRHL2 Collaborates with FOXA1 to Establish a Targetable Pathway in Endocrine Therapy-Resistant Breast Cancer	否	无	mammary cancer	breast cancer cell	E_02_0173	PCR,Western blot,Flow cytometry	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).		Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).	Immunohistochemical staining	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).			PCR,Western blot,Flow cytometry				GRHL2
31644352	chr16	28929347	28931347	CD19	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"	human	blood	High+Lowthroughput	Sepsis Induces Prolonged Epigenetic Modifications in Bone Marrow and Peripheral Macrophages Impairing Inflammation and Wound Healing	否	无	septicemia	B cell	E_01_0203	PCR, flow cytometry, immunofluorescence staining	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"		"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"	Immunohistochemical staining	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"			PCR,Flow cytometry,免疫荧光染色				CD19
31642979	chr4	184382613	184384613	IRF2	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	human	colon	High+Lowthroughput	Three functional variants were identified to affect RPS24 expression and significantly associated with risk of colorectal cancer	是	rs7071351	Colon cancer	Human colorectal carcinoma cell	E_01_0204	PCR,Flow cytometry	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	Immunohistochemical staining	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	IRF2		PCR,Flow cytometry	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).			
31642979	chr10	79066184	79068184	ZMIZ1	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	human	colon	High+Lowthroughput	Three functional variants were identified to affect RPS24 expression and significantly associated with risk of colorectal cancer	是	rs704017	Colon cancer	Human colorectal carcinoma cell	E_01_0204	PCR,Flow cytometry	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	Immunohistochemical staining	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	ZMIZ1		PCR,Flow cytometry	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.			
31642363	chr7	148804489	148806489	EZH2	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	human	connective tissue	High+Lowthroughput	Sepsis Induces Prolonged Epigenetic Modifications in Bone Marrow and Peripheral Macrophages Impairing Inflammation and Wound Healing	否	无		mesenchymal stem cell	E_01_0205	PCR,Western blot	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	EZH2		PCR,Western blot	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2			
31641208	chr16	68734197	68736197	CDH1	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	human	blood	High+Lowthroughput	Enhancer of zeste homolog 2 enhances the migration and chemotaxis of dental mesenchymal stem cells	是	rs7198799,	tumour		E_01_0206	PCR,Western blot	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	Immunohistochemical staining	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	CDH1		PCR,Western blot	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.			
31636473	chr10	67881712	67883712	SIRT1	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	human	Epithelial tissues	High+Lowthroughput	Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis	否	无		epithelial cell	E_01_0207	Flow cytometry,PCR,Western blot	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	Immunohistochemical staining	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	SIRT1		Flow cytometry,PCR,Western blot	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing			
31636429	chr5	70046788	70048788	SMN2	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).	human	Epithelial tissues	High+Lowthroughput	Structural basis of a small molecule targeting RNA for a specific splicing correction	否	无	Spinal muscular atrophy	HEK293T	E_01_0208	Western blot	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).		The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).	Immunohistochemical staining	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).			Western blot				SMN2
31636200	chr4	110614447	110616447	PITX2	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	human	connective tissue	High+Lowthroughput	Long-range Pitx2c enhancer-promoter interactions prevent predisposition to atrial fibrillation	是	rs2595104	Atrial fibrillation	embryonic stem cell	E_01_0209	Flow cytometry,PCR,Western blot	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	Immunohistochemical staining	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	PITX2		Flow cytometry,PCR,Western blot	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.			
31634421	chr16	92395428	92397428	Runx1	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.	human	blood	High+Lowthroughput	Gata3 targets Runx1 in the embryonic haematopoietic stem cell niche	否	无	Hematologic disorders	hematopoietic stem cell	E_01_0210	Flow cytometry,PCR,Western blot	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.		Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.	Immunohistochemical staining	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.			Flow cytometry,PCR,Western blot				Runx1
31633376	chr6	84684753	84686753	TBX18	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	human	Musculature	High+Lowthroughput	Transcription Factor TBX18 Reprograms Vascular Smooth Muscle Cells of Ascending Aorta to Pacemaker-Like Cells	否	无		smooth muscle cell	E_01_0211	Flow cytometry, PCR, immunofluorescence staining	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	Immunohistochemical staining	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	TBX18		Flow cytometry,PCR,免疫荧光染色	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.			
31632241	chr20	50885804	50887804	ADNP	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 	human,mouse		High+Lowthroughput	A Novel Microtubule-Tau Association Enhancer and Neuroprotective Drug Candidate: Ac-SKIP	否	无	Alzheimer		E_02_0174	Flow cytometry,PCR,Western blot	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 		Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 	Immunohistochemical staining	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 			Flow cytometry,PCR,Western blot				ADNP
31631036	chr7	148804245	148806245	EZH2	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).	human,mouse	connective tissue	High+Lowthroughput	Inhibition of EZH2 ameliorates cartilage endplate degeneration and attenuates the progression of intervertebral disc degeneration via demethylation of Sox-9	否	无	Disc degeneration	stem cell	E_02_0175	PCR,Western blot	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).		To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).	Immunohistochemical staining	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).			PCR,Western blot				EZH2
31631026	chr1	23017098	23019098	KDM1A	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	human	connective tissue	High+Lowthroughput	Re-programing Chromatin with a Bifunctional LSD1/HDAC Inhibitor Induces Therapeutic Differentiation in DIPG	否	无	Desmosomas	melanoma cells	E_01_0212	Western blot,PCR,Flow cytometry	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	Immunohistochemical staining	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	KDM1A		Western blot,PCR,Flow cytometry	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.			
31631012	chr2	209421458	209423458	MAP2	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	human	connective tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs2176546		pluripotent stem cell	E_01_0213	Flow cytometry,PCR	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).		Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Immunohistochemical staining	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).			Flow cytometry,PCR				MAP2
31631012	chr9	91560120	91562120	ROR2	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	human	connective tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs2176546		pluripotent stem cell	E_01_0213	Flow cytometry,PCR	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Immunohistochemical staining	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	ROR2		Flow cytometry,PCR	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).			
31631012	chr12	7784977	7786977	NANOG	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	human	Nervous tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs6545663		neural progenitor cell	E_01_0213	Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.		Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Immunohistochemical staining	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.			Flow cytometry,PCR				NANOG
31631012	chr6	31161576	31163576	POU5F1	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	human	Nervous tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs6545663		neural progenitor cell	E_01_0213	Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Immunohistochemical staining	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	POU5F1		Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.			
31631012	chr1	212563135	212565135	ATF3	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	human	connective tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs6545664		stem cell	E_01_0213	Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.		Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Immunohistochemical staining	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.			Flow cytometry,PCR				ATF3
31629814	chrX	47632617	47634617	ELK1	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	human	liver	High+Lowthroughput	The Dynamic Chromatin Architecture of the Regenerating Liver	否	无	Obesity	hepatocyte	E_01_0214	Flow cytometry,PCR	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	Immunohistochemical staining	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	KCNH4		Flow cytometry,PCR	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40			
31629687	chr1	35867480	35869480	AGO1	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells	human	liver	High+Lowthroughput	Nuclear AGO1 Regulates Gene Expression by Affecting Chromatin Architecture in Human Cells	否	无	cancer	HepG2 cell	E_01_0215	Western blot,Flow cytometry,PCR	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells		A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells	Immunohistochemical staining	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells			Western blot,Flow cytometry,PCR				AGO1
31628347	chr5	147234799	147236799	Cdx2	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	human	connective tissue	High+Lowthroughput	Super-enhancer-guided mapping of regulatory networks controlling mouse trophoblast stem cells	否	无		Trophoblast stem cell	E_01_0216	Flow cytometry	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.		We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Immunohistochemical staining	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.			Flow cytometry				Cdx2
31628347	chr6	128198651	128200651	Tead4	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	human	connective tissue	High+Lowthroughput	Super-enhancer-guided mapping of regulatory networks controlling mouse trophoblast stem cells	否	无		Trophoblast stem cell	E_01_0216	Flow cytometry	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.		We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Immunohistochemical staining	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.			Flow cytometry				Tead4
31628324	chr16	72780389	72782389	ZFHX3	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 	human,mouse	Musculature	High+Lowthroughput	Identification of atrial fibrillation associated genes and functional non-coding variants	是	rs281766	Arrhythmia	muscle cell	E_02_0176	Flow cytometry,PCR	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 		A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 	Immunohistochemical staining	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 			Flow cytometry,PCR				ZFHX3
31626715	chr4	108044853	108046853	LEF1	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 	human,mouse	breast	High+Lowthroughput	LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer	否	无	mammary cancer	breast cancer cell	E_02_0177	Western blot,PCR,Flow cytometry	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 		Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 	Immunohistochemical staining	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 			Western blot,PCR,Flow cytometry				LEF1
31624269	chr14	95707296	95709296	TCL1A	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.	human,mouse	blood	High+Lowthroughput	GWAS of mosaic loss of chromosome Y highlights genetic effects on blood cell differentiation	是	rs17758695		hematopoietic stem cell	E_02_0178	Flow cytometry	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.		Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.	Immunohistochemical staining	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.			Flow cytometry				TCL1A
31624086	chr6	45325657	45327657	RUNX2	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).	human,mouse	connective tissue	High+Lowthroughput	RAIN Is a Novel Enhancer-Associated lncRNA That Controls RUNX2 Expression and Promotes Breast and Thyroid Cancer	否	无	cancer	cancer cell	E_02_0179	Flow cytometry,PCR	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).		RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).	Immunohistochemical staining	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).			Flow cytometry,PCR				RUNX2
31623059	chr1	998360	1000360	ISG15	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).	human	blood	High+Lowthroughput	Identification of an Interferon-Stimulated Long Noncoding RNA (LncRNA ISR) Involved in Regulation of Influenza A Virus Replication	否	无	influenza	B cell	E_01_0217	PCR,Western blot	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).		However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).	Immunohistochemical staining	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).			PCR,Western blot				ISG15
31622687	chr3	101825749	101827749	NFKBIZ	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).	human	blood	High+Lowthroughput	IκBζ is a key player in the antipsoriatic effects of secukinumab	否	无	Psoriasis	B cell	E_01_0218	PCR,Western blot	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).		No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).	Immunohistochemical staining	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).			PCR,Western blot				NFKBIZ
31621893	chr12	6531600	6533600	GAPDH	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	human	liver	High+Lowthroughput	Costunolide represses hepatic fibrosis through WW domain-containing protein 2-mediated Notch3 degradation	否	无		hepatic stellate cell	E_01_0219	PCR, Western blot, immunofluorescence staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Immunohistochemical staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	GAPDH		PCR,Western blot,免疫荧光染色	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .			
31621893	chr6	125135892	125137892	Gapdh	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	human	kidney	High+Lowthroughput	Costunolide represses hepatic fibrosis through WW domain-containing protein 2-mediated Notch3 degradation	否	无		HEK293T	E_01_0219	PCR, Western blot, immunofluorescence staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .		The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Immunohistochemical staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .			PCR,Western blot,免疫荧光染色				Gapdh
31621133	chr17	42310525	42312525	STAT3	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	human	liver	High+Lowthroughput	Interleukin-34 mediated by hepatitis B virus X protein via CCAAT/enhancer-binding protein α contributes to the proliferation and migration of hepatoma cells	否	无	liver cancer	HCC cell	E_01_0220	PCR, gene knockdown, Western blot	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	Immunohistochemical staining	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	STAT3		PCR,基因敲降,Western blot	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.			
31620967	chr12	6531445	6533445	GAPDH	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;	mouse	heart	High+Lowthroughput	One year of exercise training promotes distinct adaptations in right and left ventricle of female Sprague-Dawley rats	否	无		Cardiac progenitor cell	E_02_0180	PCR,Western blot	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;		Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;	Immunohistochemical staining	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;			PCR,Western blot				GAPDH
31619507	chr4	147635062	147637062	PRMT9	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 	human	lung	High+Lowthroughput	PRMT6 Promotes Lung Tumor Progression via the Alternate Activation of Tumor-Associated Macrophages	否	无	tumour	NSCLC cell	E_01_0221	PCR, gene knockdown, Western blot	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 		Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 	Immunohistochemical staining	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 			PCR,基因敲降,Western blot				PRMT9
31619182	chr7	148804718	148806718	EZH2	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	human	blood	High+Lowthroughput	Inhibition of Polycomb Repressive Complex 2 activity reduces trimethylation of H3K27 and affects development in Arabidopsis seedlings	否	无	leukemia	leukemic cell	E_01_0222	PCR, Western blot, immunofluorescence staining	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	Immunohistochemical staining	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	EZH2		PCR,Western blot,免疫荧光染色	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.			
31618980	chr10	67881914	67883914	SIRT1	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	human	Musculature	High+Lowthroughput	Gynostemma Pentaphyllum Extract Ameliorates High-Fat Diet-Induced Obesity in C57BL/6N Mice by Upregulating SIRT1	否	无	Obesity	mouse cell of skeletal muscle	E_01_0223	PCR,Western blot	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	Immunohistochemical staining	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	SIRT1		PCR,Western blot	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].			
31618627	chr12	2956471	2958471	TEAD4	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	human	connective tissue	High+Lowthroughput	Activation of Oncogenic Super-Enhancers Is Coupled with DNA Repair by RAD51	否	无	cancer		E_01_0224	PCR,Flow cytometry	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	Immunohistochemical staining	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	TEAD4		PCR,Flow cytometry	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.			
31616042	chr16	54280654	54282654	IRX3	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."	human	connective tissue	High+Lowthroughput	Understanding the genetics of neuropsychiatric disorders: the potential role of genomic regulatory blocks	是	rs75059851	tumour	tumor cell	E_01_0225	Flow cytometry	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."		"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."	Immunohistochemical staining	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."			Flow cytometry				IRX3
31616042	chr2	57904994	57906994	VRK2	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.	human	Nervous tissue	High+Lowthroughput	Understanding the genetics of neuropsychiatric disorders: the potential role of genomic regulatory blocks	是	rs10791097	Schizophrenia	neural cell	E_01_0225	Flow cytometry	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.		A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.	Immunohistochemical staining	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.			Flow cytometry				VRK2
31615896	chr17	39401537	39403537	MED1	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	human	connective tissue	High+Lowthroughput	The transcription factor NKX1-2 promotes adipogenesis and may contribute to a balance between adipocyte and osteoblast differentiation	否	无	Thyroid cancer	ear mesenchymal stem cell	E_01_0226	Western blot,PCR	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	Immunohistochemical staining	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	MED1		Western blot,PCR	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.			
31615655	chr17	39458277	39460277	CDK12	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].	human,mouse	thyroid	High+Lowthroughput	Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma	否	无	Anaplastic thyroid cancer	Anaplastic thyroid carcinoma cell	E_02_0181	PCR, Western blot, flow cytometry, immunofluorescence staining	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].		CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].	Immunohistochemical staining	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].			PCR,Western blot,Flow cytometry,免疫荧光染色				CDK12
31615341	chr1	204393890	204395890	PPP1R15B	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.	human,mouse	Epithelial tissues	High+Lowthroughput	Circulatory miR-98-5p levels are deregulated during diabetes and it inhibits proliferation and promotes apoptosis by targeting PPP1R15B in keratinocytes	否	无	diabetes	HaCaT cell	E_02_0182	Flow cytometry,PCR,Western blot	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.		However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.	Immunohistochemical staining	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.			Flow cytometry,PCR,Western blot				PPP1R15B
31614133	chr5	88713906	88715906	MEF2C	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.	human,mouse	Musculature	High+Lowthroughput	CAIII expression in skeletal muscle is regulated by Ca(2+)-CaMKII-MEF2C signaling	否	无		mouse cell of skeletal muscle	E_02_0183	PCR,Western blot	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.		Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.	Immunohistochemical staining	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.			PCR,Western blot				MEF2C
31614133	chr15	99563007	99565007	MEF2A	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 	human,mouse	Musculature	High+Lowthroughput	CAIII expression in skeletal muscle is regulated by Ca(2+)-CaMKII-MEF2C signaling	否	无		C2C12 cell	E_02_0183	PCR,Western blot	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 		Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 	Immunohistochemical staining	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 			PCR,Western blot				MEF2A
31610176	chr6	131945597	131947597	CCN2	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	melanoma cells	E_01_0227	Flow cytometry,PCR,Western blot	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Immunohistochemical staining	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	CCN2		Flow cytometry,PCR,Western blot	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.			
31610176	chr3	34702118	34704118	Sox2	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	stem cell	E_01_0227	Flow cytometry,PCR,Western blot	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.		Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Immunohistochemical staining	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.			Flow cytometry,PCR,Western blot				Sox2
31610176	chr7	140716436	140718436	BRAF	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	tumor cell	E_01_0227	Flow cytometry,PCR,Western blot	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	Immunohistochemical staining	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	BRAF		Flow cytometry,PCR,Western blot	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.			
31610176	chr8	76678526	76680526	ZFHX4	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	dermal progenitor cell	E_01_0227	Flow cytometry,PCR,Western blot	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.		This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.	Immunohistochemical staining	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.			Flow cytometry,PCR,Western blot				ZFHX4
31608710	chr1	173855753	173857753	GAS5	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	human	eye	High+Lowthroughput	Silencing of GAS5 Alleviates Glaucoma in Rat Models by Reducing Retinal Ganglion Cell Apoptosis	否	无	glaucoma	retinal ganglion cell	E_01_0228	PCR, Western blot, immunofluorescence light staining, flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Immunohistochemical staining	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	GAS5		PCR,Western blot,免疫荧光光染色,Flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.			
31608710	chr7	148804386	148806386	EZH2	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	human	kidney	High+Lowthroughput	Silencing of GAS5 Alleviates Glaucoma in Rat Models by Reducing Retinal Ganglion Cell Apoptosis	否	无	glaucoma	HEK293 cell	E_01_0228	PCR, Western blot, immunofluorescence light staining, flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Immunohistochemical staining	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	EZH2		PCR,Western blot,免疫荧光光染色,Flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.			
31608710	chr9	104778194	104780194	ABCA1	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.	human	connective tissue	High+Lowthroughput	Silencing of GAS5 Alleviates Glaucoma in Rat Models by Reducing Retinal Ganglion Cell Apoptosis	否	无	glaucoma	neuroblastoma cell	E_01_0228	PCR, Western blot, immunofluorescence light staining, flow cytometry	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.		In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.	Immunohistochemical staining	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.			PCR,Western blot,免疫荧光光染色,Flow cytometry				ABCA1
31608546	chr6	88136910	88138910	CNR1	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.	human	connective tissue	High+Lowthroughput	Disease-associated polymorphisms within the conserved ECR1 enhancer differentially regulate the tissue-specific activity of the cannabinoid-1 receptor gene promoter; implications for cannabinoid pharmacogenetics	是	rs2023239	Obesity	SH-SY5Y (human neuroblastoma cell)	E_01_0229	PCR immunofluorescence staining	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.		Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.	Immunohistochemical staining	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.			PCR免疫荧光染色				CNR1
31606392	chr1	247413593	247415593	NLRP3	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].	human,mouse	blood	High+Lowthroughput	Nickel-refining fumes induce NLRP3 activation dependent on mitochondrial damage and ROS production in Beas-2B cells	否	无	inflammation	B cell	E_02_0184	PCR, Western blot, immunofluorescence staining	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].		Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].	Immunohistochemical staining	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].			PCR,Western blot,免疫荧光染色				NLRP3
31606247	chr16	30955158	30957158	SETD1A	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.	human	Nervous tissue	High+Lowthroughput	Recapitulation and Reversal of Schizophrenia-Related Phenotypes in Setd1a-Deficient Mice	是	无	Schizophrenia	neural progenitor cell	E_01_0230	Flow cytometry, PCR, immunofluorescence staining, Western blot	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.		Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.	Immunohistochemical staining	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.			Flow cytometry,PCR,免疫荧光染色,Western blot				SETD1A
31605138	chr9	21964977	21966977	CDKN2A	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	human	blood	High+Lowthroughput	Neural crest-derived tumor neuroblastoma and melanoma share 1p13.2 as susceptibility locus that shows a long-range interaction with the SLC16A1 gene	是	rs2153977	cancer		E_01_0231	Flow cytometry,PCR,Western blot	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	Immunohistochemical staining	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	CDKN2A		Flow cytometry,PCR,Western blot	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).			
31601918	chr7	44101861	44103861	AEBP1	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .	human,mouse	Nervous tissue	High+Lowthroughput	AEBP1 down regulation induced cell death pathway depends on PTEN status of glioma cells	否	无	tumour	glioma cell	E_02_0185	PCR, Western blot, immunofluorescence light staining, flow cytometry	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .		We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .	Immunohistochemical staining	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .			PCR,Western blot,免疫荧光光染色,Flow cytometry				AEBP1
31601151	chr11	35136538	35138538	CD44	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).	human,mouse	connective tissue	High+Lowthroughput	Cl- channels regulate lipid droplet formation via Rab8a expression during adipocyte differentiation	否	无		stem cell	E_02_0186	PCR, flow cytometry, Western blot, immunofluorescence staining	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).		The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).	Immunohistochemical staining	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).			PCR,Flow cytometry,Western blot,免疫荧光染色				CD44
31601151	chr1	11854664	11856664	NPPB	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).	human,mouse	connective tissue	High+Lowthroughput	Cl- channels regulate lipid droplet formation via Rab8a expression during adipocyte differentiation	否	无		3T3-L1 cell	E_02_0186	PCR, flow cytometry, Western blot, immunofluorescence staining	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).		The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).	Immunohistochemical staining	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).			PCR,Flow cytometry,Western blot,免疫荧光染色				NPPB
31599948	chr12	4365800	4367800	FGF23	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).	human	Epithelial tissues	High+Lowthroughput	A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo	否	无	cancer	epithelial cell	E_01_0232	PCR 	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).		Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).	Immunohistochemical staining	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).			PCR 				FGF23
31599948	chr20	54150645	54152645	CYP24A1	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.	human	blood	High+Lowthroughput	A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo	否	无	cancer	T cell	E_01_0232	PCR 	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.		Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.	Immunohistochemical staining	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.			PCR 				CYP24A1
31599948	chr10	126881570	126883570	Cyp27b1	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.	human	bone	High+Lowthroughput	A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo	否	无	cancer	osteocyte	E_01_0232	PCR 	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.		Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.	Immunohistochemical staining	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.			PCR 				Cyp27b1
31598701	chr7	55016371	55018371	EGFR	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.	human,mouse	breast	High+Lowthroughput	Exogenous pyruvate represses histone gene expression and inhibits cancer cell proliferation via the NAMPT-NAD+-SIRT1 pathway	否	无	mammary cancer	breast cancer cell	E_02_0187	PCR,Flow cytometry,Western blot	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.		Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.	Immunohistochemical staining	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.			PCR,Flow cytometry,Western blot				EGFR
31595632	chr12	6531857	6533857	GAPDH	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	human	connective tissue	High+Lowthroughput	The Role of miR-326 in Adipogenic Differentiation of Human Adipose-Derived Stem Cells by Targeting C/EBPα in vitro	否	无	Obesity	mesenchymal stem cell	E_01_0233	PCR, Western blot	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	Immunohistochemical staining	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	GAPDH		PCR, Western blot	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.			
31592235	chr12	57744934	57746934	CDK4	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.	mouse	Musculature	High+Lowthroughput	P21 and P27 promote tumorigenesis and progression via cell cycle acceleration in seminal vesicles of TRAMP mice	否	无	prostatic cancer	smooth muscle cell	E_02_0188	Western blot	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.		Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.	Immunohistochemical staining	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.			Western blot				CDK4
31592235	chr7	55016191	55018191	EGFR	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.	mouse	connective tissue	High+Lowthroughput	P21 and P27 promote tumorigenesis and progression via cell cycle acceleration in seminal vesicles of TRAMP mice	否	无	tumour	tumor cell	E_02_0188	Western blot	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.		The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.	Immunohistochemical staining	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.			Western blot				EGFR
31592229	chr7	148804549	148806549	EZH2	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).	human,Pig	intestine	High+Lowthroughput	Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2	否	无	Infectious gastroenteritis	porcine intestinal epthelial cell	E_02_0189	Western blot, flow cytometry, PCR, immunofluorescence staining	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).		In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).	Immunohistochemical staining	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).			Western blot,Flow cytometry,PCR,免疫荧光染色				EZH2
31592229	chr10	74821853	74823853	KAT6B	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].	human,Pig	kidney	High+Lowthroughput	Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2	否	无	cancer	PK-15 cell	E_02_0189	Western blot, flow cytometry, PCR, immunofluorescence staining	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].		miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].	Immunohistochemical staining	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].			Western blot,Flow cytometry,PCR,免疫荧光染色				KAT6B
31592229	chr2	74831204	74833204	HK2	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.	human,Pig	blood	High+Lowthroughput	Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2	否	无	cancer	B cell	E_02_0189	Western blot, flow cytometry, PCR, immunofluorescence staining	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.		However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.	Immunohistochemical staining	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.			Western blot,Flow cytometry,PCR,免疫荧光染色				HK2
31592021	chr10	100370073	100372073	OLMALINC	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.	human	liver	High+Lowthroughput	Novel Lipid Long Intervening Noncoding RNA, Oligodendrocyte Maturation-Associated Long Intergenic Noncoding RNA, Regulates the Liver Steatosis Gene Stearoyl-Coenzyme A Desaturase As an Enhancer RNA	否	无	liver cancer	HepG2 cell	E_01_0234	Flow cytometry,Western blot	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.		maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.	Immunohistochemical staining	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.			Flow cytometry,Western blot				OLMALINC
31591447	chr4	53777000	53779000	Tal2	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	human,mouse	Epithelial tissues	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无		anterior epiblast cell	E_02_0190	Flow cytometry,PCR	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes		We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Immunohistochemical staining	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes			Flow cytometry,PCR				Tal2
31591447	chr5	120566993	120568993	Lhx5	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	human,mouse	blood	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无			E_02_0190	Flow cytometry,PCR	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes		We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Immunohistochemical staining	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes			Flow cytometry,PCR				Lhx5
31591447	chr3	34701896	34703896	Sox2	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	human,mouse	connective tissue	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无		EpiSC细胞	E_02_0190	Flow cytometry,PCR	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).		These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Immunohistochemical staining	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).			Flow cytometry,PCR				Sox2
31591447	chr7	79439406	79441406	Mesp1	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	human,mouse	Musculature	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无		muscle cell	E_02_0190	Flow cytometry,PCR	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).		These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Immunohistochemical staining	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).			Flow cytometry,PCR				Mesp1
31590652	chr12	7785003	7787003	NANOG	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.	human	connective tissue	High+Lowthroughput	AIKYATAN: mapping distal regulatory elements using convolutional learning on GPU	否	无	cancer	embryonic stem cell	E_01_0235	PCR	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.		We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.	Immunohistochemical staining	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.			PCR				NANOG
31589602	chr12	80713954	80715954	MYF5	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).	human,mouse	blood	High+Lowthroughput	Dynamic enhancers control skeletal muscle identity and reprogramming	否	无	cancer	T cell	E_02_0191	Flow cytometry,PCR	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).		We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).	Immunohistochemical staining	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).			Flow cytometry,PCR				MYF5
31589096	chr17	42697169	42699169	EZH1	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.	human	nasopharynx	High+Lowthroughput	Glycyrrhiza glabra suppresses nasopharyngeal carcinoma cell proliferation through inhibiting the expression of lncRNA, AK027294	否	无	Nasopharyngeal carcinoma	nasopharyngeal carcinoma cell	E_01_0236	Western blot,Flow cytometry,PCR	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.		Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.	Immunohistochemical staining	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.			Western blot,Flow cytometry,PCR				EZH1
31588347	chr5	113018862	113020862	MCC	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.	human	Epithelial tissues	High+Lowthroughput	Benzisothiazolinone upregulates the MUC5AC expression via ERK1/2, p38, and NF-κB pathways in airway epithelial cells	否	无	asthma	epithelial cell	E_01_0237	PCR,Western blot 	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.		Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.	Immunohistochemical staining	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.			PCR,Western blot 				MCC
31588046	chr12	7785776	7787776	NANOG	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)	human	connective tissue	High+Lowthroughput	The RNA Helicase DDX6 Controls Cellular Plasticity by Modulating P-Body Homeostasis	否	无	cancer	cancer cell	E_01_0238	Flow cytometry, PCR, immunofluorescence staining	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)		After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)	Immunohistochemical staining	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)			Flow cytometry,PCR,免疫荧光染色				NANOG
31588023	chr1	170660059	170662059	PRRX1	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)	human	connective tissue	High+Lowthroughput	Histone Variant and Cell Context Determine H3K27M Reprogramming of the Enhancer Landscape and Oncogenic State	否	无	Malignancy	immune cell	E_01_0239	Flow cytometry, PCR, immunofluorescence staining	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)		Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)	Immunohistochemical staining	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)			Flow cytometry,PCR,免疫荧光染色				PRRX1
31588020	chr17	39685586	39687586	ERBB2	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).	mouse	blood	High+Lowthroughput	Pan-Cancer Landscape and Analysis of ERBB2 Mutations Identifies Poziotinib as a Clinically Active Inhibitor and Enhancer of T-DM1 Activity	否	无	cancer	Ba/F3 cell	E_02_0192	PCR,Western blot	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).		However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).	Immunohistochemical staining	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).			PCR,Western blot				ERBB2
31586130	chr3	194133931	194135931	HES1	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	human	blood	High+Lowthroughput	NRARP displays either pro- or anti-tumoral roles in T-cell acute lymphoblastic leukemia depending on Notch and Wnt signaling	否	无	Acute lymphoblastic leukemia	T cell	E_01_0240	PCR,Western blot	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	Immunohistochemical staining	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	HES1		PCR,Western blot	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).			
31586130	chr4	108044223	108046223	LEF1	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).	mouse	Nervous tissue	High+Lowthroughput	NRARP displays either pro- or anti-tumoral roles in T-cell acute lymphoblastic leukemia depending on Notch and Wnt signaling	否	无	Acute lymphoblastic leukemia	neural crest cell	E_01_0240	PCR,Western blot	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).		Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).	Immunohistochemical staining	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).			PCR,Western blot				LEF1
31586043	chr5	1389936	1391936	SLC6A3	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .	human,mouse	Nervous tissue	High+Lowthroughput	Identification of HIVEP2 as a dopaminergic transcription factor related to substance use disorders in rats and humans	是	rs67175440	Immunodeficiencies	SH-SH5Y cell	E_02_0193	PCR,Western blot	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .		Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .	Immunohistochemical staining	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .			PCR,Western blot				SLC6A3
31586043	chr10	102227203	102229203	PITX3	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.	human,mouse	Nervous tissue	High+Lowthroughput	Identification of HIVEP2 as a dopaminergic transcription factor related to substance use disorders in rats and humans	是	rs748209	Immunodeficiencies	SK-N-AS cell	E_02_0193	PCR,Western blot	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.		Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.	Immunohistochemical staining	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.			PCR,Western blot				PITX3
31586032	chr16	67559931	67561931	CTCF	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.	mouse	tumour	High+Lowthroughput	The transcription factor PU.1 mediates enhancer-promoter looping that is required for IL-1β eRNA and mRNA transcription in mouse melanoma and macrophage cell lines	否	无	tumour	melanoma cells	E_02_0194	PCR,Western blot,Flow cytometry	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.		Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.	Immunohistochemical staining	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.			PCR,Western blot,Flow cytometry				CTCF
31585804	chrX	100840244	100842244	NOX1	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).	mouse	Epithelial tissues	High+Lowthroughput	Sildenafil Protects Endothelial Cells From Radiation-Induced Oxidative Stress	否	无	atherosclerosis	endothelial cell	E_02_0195	PCR	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).		Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).	Immunohistochemical staining	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).			PCR				NOX1
31585741	chrX	48506512	48508512	PORCN	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney	mouse	bone	High+Lowthroughput	Opposing actions of renal tubular- and myeloid-derived porcupine in obstruction-induced?kidney fibrosis	否	无		infiltrating myeloid cell	E_02_0196	PCR,Western blot	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney		To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney	Immunohistochemical staining	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney			PCR,Western blot				PORCN
31585741	chr11	108808537	108810537	Axin2	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.	mouse	Epithelial tissues	High+Lowthroughput	Opposing actions of renal tubular- and myeloid-derived porcupine in obstruction-induced?kidney fibrosis	否	无	Renal fibrosis	epithelial cell	E_02_0196	PCR,Western blot	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.		Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.	Immunohistochemical staining	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.			PCR,Western blot				Axin2
31584754	chr3	41191952	41193952	CTNNB1	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	human	tumour	High+Lowthroughput	The usefulness of lymphoid enhancer-binding factor 1 and androgen receptor in diagnosing solid pseudopapillary neoplasm of the pancreas on cytopathology	否	无	tumour	tumor cell	E_01_0241	Immunohistochemistry	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	Immunohistochemical staining	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	CTNNB1		免疫组化	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1			
31583122	chr11	35136216	35138216	CD44	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.	human	lung	High+Lowthroughput	Targeting Wnt/EZH2/microRNA-708 signaling pathway inhibits neuroendocrine differentiation in prostate cancer	否	无	Lung adenocarcinoma	adenocarcinoma cell	E_01_0242	PCR,Western blot	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.		It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.	Immunohistochemical staining	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.			PCR,Western blot				CD44
31582835	chr7	148804794	148806794	EZH2	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	human	tumour	High+Lowthroughput	EZH2 targeting reduces medulloblastoma growth through epigenetic reactivation of the BAI1/p53 tumor suppressor pathway	否	无	Medulloblastoma	Medulloblastoma cell	E_01_0243	PCR,Western blot	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	Immunohistochemical staining	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	EZH2		PCR,Western blot	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.			
31581708	chr17	39726151	39728151	MIEN1	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.	human	prostate	High+Lowthroughput	Migration and Invasion Enhancer 1 Is an NF-?B-Inducing Gene Enhancing the Cell Proliferation and Invasion Ability of Human Prostate Carcinoma Cells In Vitro and In Vivo	否	无	prostatic cancer	prostate cancer cell	E_01_0244	PCR,Western blot,Flow cytometry	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.		Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.	Immunohistochemical staining	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.			PCR,Western blot,Flow cytometry				MIEN1
31581708	chr8	133234553	133236553	NDRG1	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].	human	Epithelial tissues	High+Lowthroughput	Migration and Invasion Enhancer 1 Is an NF-?B-Inducing Gene Enhancing the Cell Proliferation and Invasion Ability of Human Prostate Carcinoma Cells In Vitro and In Vivo	否	无	prostatic cancer	epithelial cell	E_01_0244	PCR,Western blot,Flow cytometry	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].		Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].	Immunohistochemical staining	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].			PCR,Western blot,Flow cytometry				NDRG1
31581661	chr8	127733019	127735019	MYC	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	human	prostate	High+Lowthroughput	Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells	否	无	prostatic cancer	prostate cancer cell	E_01_0245	PCR 	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	Immunohistochemical staining	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	MYC		PCR 	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.			
31579944	chr7	148804427	148806427	EZH2	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.	human,mouse	Epithelial tissues	High+Lowthroughput	Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis	否	无	cancer	peritoneal mesothelial cell	E_02_0197	PCR, Western blot, immunofluorescence staining	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.		Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.	Immunohistochemical staining	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.			PCR,Western blot,免疫荧光染色				EZH2
31579944	chr17	78850292	78852292	TIMP2	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 	human,mouse	connective tissue	High+Lowthroughput	Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis	否	无	inflammation	Inflammatory cell	E_02_0197	PCR, Western blot, immunofluorescence staining	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 		Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 	Immunohistochemical staining	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 			PCR,Western blot,免疫荧光染色				TIMP2
31579944	chr17	42310753	42312753	STAT3	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].	human,mouse	pancreas	High+Lowthroughput	Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis	否	无	pancreatic cancer	pancreatic cancer cell	E_02_0197	PCR, Western blot, immunofluorescence staining	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].		Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].	Immunohistochemical staining	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].			PCR,Western blot,免疫荧光染色				STAT3
31579913	chr20	63192571	63194571	YTHDF1	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				YTHDF1
31579913	chr8	63165861	63167861	YTHDF3	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				YTHDF3
31579913	chr1	28734326	28736326	YTHDF2	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				YTHDF2
31579913	chr10	119031225	119033225	EIF3A	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				EIF3A
31579098	chr7	148804077	148806077	EZH2	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	human	tumour	High+Lowthroughput	DZNep inhibits Hif-1α and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells	否	无	tumour	tumor cell	E_01_0247	PCR,Western blot,Flow cytometry	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	Immunohistochemical staining	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	EZH2		PCR,Western blot,Flow cytometry	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.			
31575636	chr22	41830453	41832453	SREBF2	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).	human,mouse		High+Lowthroughput	Regeneration Rosetta: An Interactive Web Application To Explore Regeneration-Associated Gene Expression and Chromatin Accessibility	否	无			E_02_0198	RNA-seq	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).		Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).	Immunohistochemical staining	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).			RNA-seq				SREBF2
31573688	chr12	16545165	16547165	LMO3	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).	human	connective tissue	High+Lowthroughput	Resveratrol Inhibits Human Visceral Preadipocyte Proliferation and Differentiation in vitro	否	无	diabetes	3T3-L1 cell	E_01_0248	PCR,Western blot	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).		LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).	Immunohistochemical staining	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).			PCR,Western blot				LMO3
31572429	chr22	41558440	41560440	CSDC2	Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.	human	breast	High+Lowthroughput	Purification and Identification of miRNA Target Sites in Genome Using DNA Affinity Precipitation	否	无	mammary cancer	MCF-7 cell	E_01_0249		Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.		Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.	Immunohistochemical staining	Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.							CSDC2
31571902	chr22	15781801	15783801	DUXAP8	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.	human	liver	High+Lowthroughput	Up-regulated long non-coding RNA DUXAP8 promotes cell growth through repressing Krüppel-like factor 2 expression in human hepatocellular carcinoma	否	无	liver cancer	hepatocellular carcinoma cell	E_01_0250	PCR	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.		Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.	Immunohistochemical staining	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.			PCR				DUXAP8
31570750	chr1	10633990	10635990	CASZ1	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.	human	kidney	High+Lowthroughput	A variant of the castor zinc finger 1 (CASZ1) gene is differentially associated with the clinical classification of chronic venous disease	是	rs11121615	Chronic venous disease	HEK293 cell	E_01_0251	PCR,Flow cytometry	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.		This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.	Immunohistochemical staining	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.			PCR,Flow cytometry				CASZ1
31570746	chr13	40553093	40555093	FOXO1	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	human	connective tissue	High+Lowthroughput	Characterization of the Long Terminal Repeat of the Endogenous Retrovirus-derived microRNAs in the Olive Flounder	否	无	cancer	cancer cell	E_01_0252	PCR	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	Immunohistochemical staining	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	FOXO1		PCR	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated			
31570000	chr19	10651535	10653535	ILF3	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.	human,mouse		High+Lowthroughput	The RNA-binding protein ILF3 binds to transposable element sequences in SINEUP lncRNAs	否	无	liver cancer	DH5a cells	E_02_0199	Western blot,Flow cytometry,PCR	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.		The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.	Immunohistochemical staining	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.			Western blot,Flow cytometry,PCR				ILF3
31563853	chr3	186840138	186842138	ADIPOQ	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)	human	Fat	High+Lowthroughput	CIDEA Transcriptionally Regulates UCP1 for Britening and Thermogenesis in Human Fat Cells	否	无		fat cell	E_01_0253	Western blot, flow cytometry, PCR, immunofluorescence staining	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)		Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)	Immunohistochemical staining	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)			Western blot,Flow cytometry,PCR,免疫荧光染色				ADIPOQ
31563432	chr4	154747879	154749879	Actrt2	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).	human	colon	High+Lowthroughput	Mediator Condensates Localize Signaling Factors to Key Cell Identity Genes	否	无	Colon cancer	HCT116 cells	E_01_0254	Immunofluorescence light staining, flow cytometry, PCR	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).		Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).	Immunohistochemical staining	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).			免疫荧光光染色,Flow cytometry,PCR				Actrt2
31563432	chr17	42310179	42312179	STAT3	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	human	kidney	High+Lowthroughput	Mediator Condensates Localize Signaling Factors to Key Cell Identity Genes	否	无		HEK293T	E_01_0254	Immunofluorescence light staining, flow cytometry, PCR	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	Immunohistochemical staining	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	STAT3		免疫荧光光染色,Flow cytometry,PCR	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).			
31562697	chr3	69736600	69738600	MITF	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.	human,mouse	connective tissue	High+Lowthroughput	Delineating the role of MITF isoforms in pigmentation and tissue homeostasis	否	无	Melanoma	Pigment Cell	E_02_0200	PCR, Western blot, immunofluorescence staining	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.		MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.	Immunohistochemical staining	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.			PCR,Western blot,免疫荧光染色				MITF
31562697	chr11	89175705	89177705	TYR	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).	human,mouse	breast	High+Lowthroughput	Delineating the role of MITF isoforms in pigmentation and tissue homeostasis	否	无	mammary cancer	breast cancer stem cell 	E_02_0200	PCR, Western blot, immunofluorescence staining	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).		We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).	Immunohistochemical staining	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).			PCR,Western blot,免疫荧光染色				TYR
31561451	chr7	55016281	55018281	EGFR	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	human	connective tissue	High+Lowthroughput	Fluorescein- and EGFR-Antibody Conjugated Silica Nanoparticles for Enhancement of Real-time Tumor Border Definition Using Confocal Laser Endomicroscopy in Squamous Cell Carcinoma of the Head and Neck	否	无	tumour	squamous cell	E_01_0255	PCR, Western blot, immunofluorescence staining	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	Immunohistochemical staining	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	EGFR		PCR,Western blot,免疫荧光染色	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.			
31561366	chr11	47463063	47465063	CELF1	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.	human	blood	High+Lowthroughput	Fluorescein- and EGFR-Antibody Conjugated Silica Nanoparticles for Enhancement of Real-time Tumor Border Definition Using Confocal Laser Endomicroscopy in Squamous Cell Carcinoma of the Head and Neck	是	rs8093731	Chronic myeloid leukemia	K562  cells	E_01_0256	PCR,Flow cytometry	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.		The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.	Immunohistochemical staining	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.			PCR,Flow cytometry				CELF1
31561366	chr14	52854332	52856332	FERMT2	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).	human	connective tissue	High+Lowthroughput	Inferring the Molecular Mechanisms of Noncoding Alzheimer's Disease-Associated Genetic Variants	是	rs4543938	Chronic myeloid leukemia	monocyte cells	E_01_0256	PCR,Flow cytometry	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).		Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).	Immunohistochemical staining	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).			PCR,Flow cytometry				FERMT2
31560287	chr11	116832779	116834779	APOA1	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].	human	Fat	High+Lowthroughput	New Insights into Apolipoprotein A5 and the Modulation of Human Adipose-derived Mesenchymal Stem Cells Adipogenesis	是	无	Obesity	adipose-derived mesenchymal stem cells	E_01_0257	PCR,Western blot	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].		Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].	Immunohistochemical staining	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].			PCR,Western blot				APOA1
31558567	chrX	47579564	47581564	TIMP1	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.	human,mouse	bone	High+Lowthroughput	Hippo pathway deletion in adult resting cardiac fibroblasts initiates a cell state transition with spontaneous and self-sustaining fibrosis	否	无	miocardial infarction	myeloid cell	E_02_0201	PCR, flow cytometry, gene knockdown	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.		Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.	Immunohistochemical staining	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.			PCR,Flow cytometry,基因敲降				TIMP1
31557715	chr7	25947403	25949403	MIR148A	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes	human	connective tissue	High+Lowthroughput	Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation	是	rs1055144	liver cancer	mesenchymal stem cell	E_01_0258	PCR, flow cytometry, immunofluorescence staining	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes		Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes	Immunohistochemical staining	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes			PCR,Flow cytometry,免疫荧光染色				MIR148A
31557715	chr7	26288944	26290944	SNX10	The region is delimited by the distal gene NPVF and the proximal gene SNX10.	human	Fat	High+Lowthroughput	Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation	是	rs7798002	liver cancer	SGBS cells	E_01_0258	PCR, flow cytometry, immunofluorescence staining	The region is delimited by the distal gene NPVF and the proximal gene SNX10.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The region is delimited by the distal gene NPVF and the proximal gene SNX10.		The region is delimited by the distal gene NPVF and the proximal gene SNX10.	Immunohistochemical staining	The region is delimited by the distal gene NPVF and the proximal gene SNX10.			PCR,Flow cytometry,免疫荧光染色				SNX10
31557715	chr1	203176161	203178161	CHI3L1	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.	human	liver cancer	High+Lowthroughput	Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation	是	rs1451385	liver cancer	HepG2 cell	E_01_0258	PCR, flow cytometry, immunofluorescence staining	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.		RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.	Immunohistochemical staining	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.			PCR,Flow cytometry,免疫荧光染色				CHI3L1
31554806	chr1	37806934	37808934	MTF1	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome	human	breast	High+Lowthroughput	Chromatin-informed inference of transcriptional programs in gynecologic and basal breast cancers	否	无	mammary cancer	breast cancer cell	E_01_0259	Flow cytometry	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome		PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome	Immunohistochemical staining	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome			Flow cytometry				MTF1
31551362	chr3	181709186	181711186	SOX2	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).	human,mouse	lung	High+Lowthroughput	Epigenomic Profiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	是	无	Lung squamous cell carcinoma	Lung squamous cell	E_02_0202	PCR, Western blot, flow cytometry, immunofluorescence staining	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).		We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).	Immunohistochemical staining	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).			PCR,Western blot,Flow cytometry,免疫荧光染色				SOX2
31551362	chr6	98831871	98833871	POU3F2	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.	human,mouse	kidney	High+Lowthroughput	Epigenomic Profiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	是	无		HEK293T	E_02_0202	PCR, Western blot, flow cytometry, immunofluorescence staining	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.		For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.	Immunohistochemical staining	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.			PCR,Western blot,Flow cytometry,免疫荧光染色				POU3F2
31551335	chr12	55963742	55965742	CDK2	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.	human	blood	High+Lowthroughput	The Long Noncoding RNA HEAL Regulates HIV-1 Replication through Epigenetic Regulation of the HIV-1 Promoter	否	无	AIDS	blood mononuclear cells	E_01_0260	Western blot,PCR	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.		HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.	Immunohistochemical staining	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.			Western blot,PCR				CDK2
31551335	chr11	65419837	65421837	NEAT1	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs	human	blood	High+Lowthroughput	The Long Noncoding RNA HEAL Regulates HIV-1 Replication through Epigenetic Regulation of the HIV-1 Promoter	否	无	AIDS	T cell	E_01_0260	Western blot,PCR	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs		The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs	Immunohistochemical staining	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs			Western blot,PCR				NEAT1
31551256	chr9	134027777	134029777	BRD3	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.	human	breast	High+Lowthroughput	Distinct Roles for BET Family Members in Estrogen Receptor α Enhancer Function and Gene Regulation in Breast Cancer Cells	否	无	mammary cancer	breast cancer cell	E_01_0261	Western blot,PCR,Flow cytometry	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.		BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.	Immunohistochemical staining	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.			Western blot,PCR,Flow cytometry				BRD3
31551012	chr7	148804569	148806569	EZH2	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	human	stomach	High+Lowthroughput	HOXD-AS1 confers cisplatin resistance in gastric cancer through epigenetically silencing PDCD4 via recruiting EZH2	否	无	gastric cancer	gastric cancer cell	E_01_0262	Western blot,PCR	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Immunohistochemical staining	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	EZH2		Western blot,PCR	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells			
31551012	chr10	110869187	110871187	PDCD4	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	human	stomach	High+Lowthroughput	HOXD-AS1 confers cisplatin resistance in gastric cancer through epigenetically silencing PDCD4 via recruiting EZH2	否	无	gastric cancer	gastric cancer cell	E_01_0262	Western blot,PCR	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells		Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Immunohistochemical staining	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells			Western blot,PCR				PDCD4
31550664	chr17	13222491	13224491	Sod2	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].	human,mouse	pancreas	High+Lowthroughput	Gestational oxidative stress protects against adult obesity and insulin resistance	否	无	Pancreatic β - cell dysfunction	Beta cell	E_02_0203	PCR	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].		Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].	Immunohistochemical staining	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].			PCR				Sod2
31548608	chr9	107481891	107483891	KLF4	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	human,mouse	connective tissue	High+Lowthroughput	KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks	否	无		pluripotent stem cell	E_02_0204	Western blot,PCR,Flow cytometry	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22		The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Immunohistochemical staining	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22			Western blot,PCR,Flow cytometry				KLF4
31548608	chr17	35814159	35816159	Pou5f1	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	human,mouse	connective tissue	High+Lowthroughput	KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks	否	无		pluripotent stem cell	E_02_0204	Western blot,PCR,Flow cytometry	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22		The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Immunohistochemical staining	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22			Western blot,PCR,Flow cytometry				Pou5f1
31548608	chr4	56645505	56647505	HOPX	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	human,mouse	connective tissue	High+Lowthroughput	KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks	否	无		pluripotent stem cell	E_02_0204	Western blot,PCR,Flow cytometry	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22		The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Immunohistochemical staining	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22			Western blot,PCR,Flow cytometry				HOPX
31547883	chr16	67559930	67561930	CTCF	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	human	kidney	High+Lowthroughput	CGGBP1 regulates CTCF occupancy at repeats	否	无		HEK293T	E_01_0263	Flow cytometry,PCR	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	Immunohistochemical staining	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	CTCF		Flow cytometry,PCR	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).			
31547433	chr13	40553074	40555074	FOXO1	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.	human,mouse	connective tissue	High+Lowthroughput	Transcriptional Analysis of FOXO1, C/EBP-α and PPAR-γ2 Genes and Their Association with Obesity-Related Insulin Resistance	否	无	Obesity	NIH-3T3 fibroblastic cell	E_02_0205	Western blot,PCR	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.		The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.	Immunohistochemical staining	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.			Western blot,PCR				FOXO1
31546863	chr11	36480909	36482909	TRAF6	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm	mouse	blood	High+Lowthroughput	Egg White Ovotransferrin Attenuates RANKL-Induced Osteoclastogenesis and Bone Resorption	否	无	osteoporosis	B cell	E_02_0206	Western blot,PCR	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm		sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm	Immunohistochemical staining	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm			Western blot,PCR				TRAF6
31546763	chr4	77508709	77510709	CXCL13	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.	human,mouse	blood	High+Lowthroughput	Heightened TLR7/9-Induced IL-10 and CXCL13 Production with Dysregulated NF-?B Activation in CD11c(hi)CD11b(+) Dendritic Cells in NZB/W F1 Mice	否	无	Systemic lupus erythematosus	T cell	E_02_0207	Western blot,PCR,Flow cytometry	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.		During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.	Immunohistochemical staining	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.			Western blot,PCR,Flow cytometry				CXCL13
31546150	chr16	68734373	68736373	CDH1	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.	human,mouse	pancreas	High+Lowthroughput	Menin Coordinates C/EBPβ-Mediated TGF-β Signaling for Epithelial-Mesenchymal Transition and Growth Inhibition in Pancreatic Cancer	否	无	Pancreatic ductal adenocarcinoma	PANC1 cells	E_02_0208	Western blot,PCR,Flow cytometry	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.		EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.	Immunohistochemical staining	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.			Western blot,PCR,Flow cytometry				CDH1
31546122	chr11	120694060	120696060	Fasn	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	mouse	connective tissue	High+Lowthroughput	Promoting differentiation and lipid metabolism are the primary effects for DINP exposure on 3T3-L1 preadipocytes	否	无		3T3-L1 cell	E_02_0209	PCR,Western blot,Flow cytometry	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).		We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Immunohistochemical staining	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).			PCR,Western blot,Flow cytometry				Fasn
31546122	chr16	22962769	22964769	Adipoq	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	mouse	kidney	High+Lowthroughput	Promoting differentiation and lipid metabolism are the primary effects for DINP exposure on 3T3-L1 preadipocytes	否	无		HEK-293T cells	E_02_0209	PCR,Western blot,Flow cytometry	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).		We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Immunohistochemical staining	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).			PCR,Western blot,Flow cytometry				Adipoq
31545422	chr7	148804556	148806556	EZH2	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	human	neck	High+Lowthroughput	Targeting of EZH2 inhibits epithelial?mesenchymal transition in head and neck squamous cell carcinoma via regulating the STAT3/VEGFR2 axis	否	无	cancer	neck squamous cell	E_01_0264	PCR, Western blot, immunofluorescence staining	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	Immunohistochemical staining	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	EZH2		PCR,Western blot,免疫荧光染色	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.			
31545422	chr17	42310472	42312472	STAT3	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	human	Head, neck	High+Lowthroughput	Targeting of EZH2 inhibits epithelial?mesenchymal transition in head and neck squamous cell carcinoma via regulating the STAT3/VEGFR2 axis	否	无	cancer	HNSCC cells	E_01_0264	PCR, Western blot, immunofluorescence staining	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	Immunohistochemical staining	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	STAT3		PCR,Western blot,免疫荧光染色	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.			
31544892	chr13	30453885	30455885	HMGB1	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.	human,Hamster	ovary	High+Lowthroughput	Enhancers Improve the AID-Induced Hypermutation in Episomal Vector for Antibody Affinity Maturation in Mammalian Cell Display	否	无	cancer	CHO cells	E_02_0210	Flow cytometry	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.		In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.	Immunohistochemical staining	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.			Flow cytometry				HMGB1
31542774	chr19	29809345	29811345	CCNE1	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	human	blood	High+Lowthroughput	Integrated paired-end enhancer profiling and whole-genome sequencing reveals recurrent CCNE1 and IGF2 enhancer hijacking in primary gastric adenocarcinoma	否	无	gastric cancer	B cell	E_01_0265	PCR,Flow cytometry	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	Immunohistochemical staining	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	CCNE1		PCR,Flow cytometry	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.			
31541592	chr6	35570844	35572844	FKBP5	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.	human	bone	High+Lowthroughput	Amyloid precursor protein, an androgen-regulated gene, is targeted by RNA-binding protein PSF/SFPQ in neuronal cells	否	无	Osteoma	SH‐SY5Y cells	E_01_0266	PCR,Western blot	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.		We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.	Immunohistochemical staining	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.			PCR,Western blot				FKBP5
31538139	chr3	186839743	186841743	ADIPOQ	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.	human	Fat	High+Lowthroughput	Reverse gene-environment interaction approach to identify variants influencing body-mass index in humans	是	rs10788522		fat cell	E_01_0267	PCR,Flow cytometry	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.		The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.	Immunohistochemical staining	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.			PCR,Flow cytometry				ADIPOQ
31536603	chr22	43148768	43150768	TSPO	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation	human,mouse	Nervous tissue	High+Lowthroughput	Lipopolysaccharide induces mouse translocator protein (18 kDa) expression via the AP-1 complex in the microglial cell line, BV-2	否	无	Neuroinflammation	microglial cell	E_02_0211	PCR, Western blot, immunofluorescence staining	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation		The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation	Immunohistochemical staining	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation			PCR,Western blot,免疫荧光染色				TSPO
31536603	chr1	32289598	32291598	HDAC1	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.	human,mouse	connective tissue	High+Lowthroughput	Lipopolysaccharide induces mouse translocator protein (18 kDa) expression via the AP-1 complex in the microglial cell line, BV-2	否	无	Neuroinflammation	immune cell	E_02_0211	PCR, Western blot, immunofluorescence staining	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.		In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.	Immunohistochemical staining	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.			PCR,Western blot,免疫荧光染色				HDAC1
31535083	chr6	90460328	90462328	Aldh1l1	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	human,mouse	Epithelial tissues	High+Lowthroughput	Genomic and epigenomic mapping of leptin-responsive neuronal populations involved in body weight regulation	是	rs11804091	Obesity	endothelial cell	E_02_0212	Immunofluorescence staining, chip, flow cytometry	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).		We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Immunohistochemical staining	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).			免疫荧光染色,CHIP,Flow cytometry				Aldh1l1
31535083	chr9	119727541	119729541	Cx3cr1	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	human,mouse	tumour	High+Lowthroughput	Genomic and epigenomic mapping of leptin-responsive neuronal populations involved in body weight regulation	是	rs11804091	Obesity	tumor cell	E_02_0212	Immunofluorescence staining, chip, flow cytometry	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).		We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Immunohistochemical staining	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).			免疫荧光染色,CHIP,Flow cytometry				Cx3cr1
31534142	chr16	67559649	67561649	CTCF	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	human	kidney	High+Lowthroughput	Epigenome editing strategies for the functional annotation of CTCF insulators	否	无	tumour	HEK293 cell	E_01_0268	PCR,Flow cytometry	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	Immunohistochemical staining	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	CTCF		PCR,Flow cytometry	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).			
31534142	chr4	54096948	54098948	GSX2	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	human		High+Lowthroughput	Epigenome editing strategies for the functional annotation of CTCF insulators	否	无	tumour		E_01_0268	PCR,Flow cytometry	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.		We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Immunohistochemical staining	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.			PCR,Flow cytometry				GSX2
31534142	chr4	54226570	54228570	PDGFRA	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	human		High+Lowthroughput	Epigenome editing strategies for the functional annotation of CTCF insulators	否	无	tumour		E_01_0268	PCR,Flow cytometry	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Immunohistochemical staining	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	PDGFRA		PCR,Flow cytometry	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.			
31533028	chr21	34785012	34787012	RUNX1	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	human	blood	High+Lowthroughput	RUNX1-ETO Depletion in t(8;21) AML Leads to C/EBPα- and AP-1-Mediated Alterations in Enhancer-Promoter Interaction	否	无	leukemia	hematopoietic stem cell	E_01_0269	PCR,Flow cytometry	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	Immunohistochemical staining	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	RUNX1		PCR,Flow cytometry	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.			
31533028	chr12	4266618	4268618	CCND2	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).	human	blood	High+Lowthroughput	RUNX1-ETO Depletion in t(8;21) AML Leads to C/EBPα- and AP-1-Mediated Alterations in Enhancer-Promoter Interaction	否	无	leukemia	Kasumi-1 cells	E_01_0269	PCR,Flow cytometry	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).		Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).	Immunohistochemical staining	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).			PCR,Flow cytometry				CCND2
31531679	chr16	86564387	86566387	FOXC2	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	human	Epithelial tissues	High+Lowthroughput	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes	否	无		epithelial cell	E_01_0270	PCR, Western blot, immunofluorescence staining	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	Immunohistochemical staining	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	FOXC2		PCR,Western blot,免疫荧光染色	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.			
31531679	chr1	179548051	179550051	NPHS2	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].	human	Epithelial tissues	High+Lowthroughput	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes	否	无		epithelial cell	E_01_0270	PCR, Western blot, immunofluorescence staining	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].		As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].	Immunohistochemical staining	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].			PCR,Western blot,免疫荧光染色				NPHS2
31531679	chr16	86527297	86529297	MTHFSD	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.	human	Epithelial tissues	High+Lowthroughput	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes	否	无		epithelial cell	E_01_0270	PCR, Western blot, immunofluorescence staining	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.		Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.	Immunohistochemical staining	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.			PCR,Western blot,免疫荧光染色				MTHFSD
31530818	chr8	127732403	127734403	MYC	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	human	blood	High+Lowthroughput	Identification of significant chromatin contacts from HiChIP data by FitHiChIP	否	无	leukemia	T cell	E_01_0271	Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Immunohistochemical staining	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	MYC		Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.			
31530818	chr17	7659021	7661021	TP53	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	human	blood	High+Lowthroughput	Identification of significant chromatin contacts from HiChIP data by FitHiChIP	否	无	leukemia	K562 cell	E_01_0271	Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Immunohistochemical staining	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	TP53		Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.			
31530812	chr2	24200308	24202308	ITSN2	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).	human	Nervous tissue	High+Lowthroughput	Long-read assembly of the Chinese rhesus macaque genome and identification of ape-specific structural variants	是	无		neuronal cell	E_01_0272	Flow cytometry,Western blot	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).		In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).	Immunohistochemical staining	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).			Flow cytometry,Western blot				ITSN2
31530812	chr6	11180134	11182134	NEDD9	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression	human	connective tissue	High+Lowthroughput	Long-read assembly of the Chinese rhesus macaque genome and identification of ape-specific structural variants	是	无		male germ cells	E_01_0272	Flow cytometry,Western blot	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression		Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression	Immunohistochemical staining	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression			Flow cytometry,Western blot				NEDD9
31530225	chr16	53698982	53700982	FTO	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids	human	connective tissue	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs9927317	Obesity	mesenchymal stem cell	E_01_0273	Flow cytometry	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids		FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids	Immunohistochemical staining	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids			Flow cytometry				FTO
31530225	chr16	53595395	53597395	RPGRIP1L	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.	human	connective tissue	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs62033405	Obesity	mesenchymal stem cell	E_01_0273	Flow cytometry	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.		The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.	Immunohistochemical staining	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.			Flow cytometry				RPGRIP1L
31530225	chr7	101813374	101815374	CUX1	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	human	Fat	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs9939609	Obesity	white adipocytes	E_01_0273	Flow cytometry	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	Immunohistochemical staining	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	CUX1		Flow cytometry	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).			
31530225	chr16	54280685	54282685	IRX3	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	human	Fat	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs8050136	Obesity	white adipocytes	E_01_0273	Flow cytometry	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.		Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Immunohistochemical staining	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.			Flow cytometry				IRX3
31530225	chr16	54928124	54930124	IRX5	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	human	Fat	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs9930506	Obesity	white adipocytes	E_01_0273	Flow cytometry	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.		Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Immunohistochemical staining	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.			Flow cytometry				IRX5
31530015	chr16	23577727	23579727	NDUFAB1	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).	human,mouse	connective tissue	High+Lowthroughput	NDUFAB1 protects against obesity and insulin resistance by enhancing mitochondrial metabolism	否	无	insulin resistance 	murine embryonic stem (ES) cell	E_02_0213	PCR,Western blot	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).		A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).	Immunohistochemical staining	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).			PCR,Western blot				NDUFAB1
31529763	chr17	43041465	43043465	BRCA1	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	human		High+Lowthroughput	(19) F?NMR Spectroscopy Tagging and Paramagnetic Relaxation Enhancement-Based Conformation Analysis of Intrinsically Disordered Protein Complexes	否	无	tumour	E-coli cell	E_01_0274	Flow cytometry	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	Immunohistochemical staining	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	BRCA1		Flow cytometry	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.			
31525599	chr11	10302280	10304280	ADM	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.	human		High+Lowthroughput	Tracing upconversion nanoparticle penetration in human skin	否	无			E_01_0275	PCR, immunofluorescence staining	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.		ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.	Immunohistochemical staining	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.			PCR,免疫荧光染色				ADM
31521883	chr18	63120882	63122882	BCL2	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	human	blood	High+Lowthroughput	Trehalose supplementation during porcine oocytes in?vitro maturation improves the developmental capacity of parthenotes	否	无		B cell	E_01_0276	PCR, immunofluorescence staining	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	Immunohistochemical staining	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	BCL2		PCR,免疫荧光染色	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.			
31521109	chr11	58037956	58039956	VN2R9P	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]	human,mouse	blood	High+Lowthroughput	A purely bioinformatic pipeline for the prediction of mammalian odorant receptor gene enhancers	否	无		T cell	E_02_0214	PCR	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]		For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]	Immunohistochemical staining	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]			PCR				VN2R9P
31520529	chr1	156461014	156463014	MEF2D	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).	mouse	Nervous tissue	High+Lowthroughput	Salidroside protects dopaminergic neurons by regulating the mitochondrial MEF2D-ND6 pathway in the MPTP/MPP(+) -induced model of Parkinson's disease	是	无	Parkinson	SN4741 cells	E_02_0215	PCR, immunofluorescence staining, Western blot	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).		Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).	Immunohistochemical staining	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).			PCR,免疫荧光染色,Western blot				MEF2D
31519749	chr3	142303842	142305842	XRN1	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.	human		High+Lowthroughput	Zika virus noncoding sfRNAs sequester multiple host-derived RNA-binding proteins and modulate mRNA decay and splicing during infection	否	无	Villous carcinoma	choriocarcinoma cells	E_01_0277	PCR,Western blot	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.		Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.	Immunohistochemical staining	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.			PCR,Western blot				XRN1
31519704	chr9	136491964	136493964	NOTCH1	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	human,mouse	blood	High+Lowthroughput	GATA3-Controlled Nucleosome Eviction Drives MYC Enhancer Activity in T-cell Development and Leukemia	否	无	leukemia	T cell	E_02_0216	PCR,Flow cytometry	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.		MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Immunohistochemical staining	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.			PCR,Flow cytometry				NOTCH1
31519704	chr8	127732540	127734540	MYC	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	human,mouse	blood	High+Lowthroughput	GATA3-Controlled Nucleosome Eviction Drives MYC Enhancer Activity in T-cell Development and Leukemia	否	无	leukemia	T cell	E_02_0216	PCR,Flow cytometry	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.		MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Immunohistochemical staining	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.			PCR,Flow cytometry				MYC
31519520	chr16	67560000	67562000	CTCF	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).	human,mouse	connective tissue	High+Lowthroughput	Transcription Factor-Directed Re-wiring of Chromatin Architecture for Somatic Cell Nuclear Reprogramming toward trans-Differentiation	否	无		somatic cell	E_02_0217	PCR, Western blot, flow cytometry, immunofluorescence staining	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).		Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).	Immunohistochemical staining	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).			PCR,Western blot,Flow cytometry,免疫荧光染色				CTCF
31519520	chr12	55681811	55683811	ITGA7	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).	human,mouse	bone	High+Lowthroughput	Transcription Factor-Directed Re-wiring of Chromatin Architecture for Somatic Cell Nuclear Reprogramming toward trans-Differentiation	否	无		mouse cell of skeletal muscle	E_02_0217	PCR, Western blot, flow cytometry, immunofluorescence staining	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).		Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).	Immunohistochemical staining	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).			PCR,Western blot,Flow cytometry,免疫荧光染色				ITGA7
31519520	chr1	201356451	201358451	TNNT2	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).	human,mouse	lung	High+Lowthroughput	Transcription Factor-Directed Re-wiring of Chromatin Architecture for Somatic Cell Nuclear Reprogramming toward trans-Differentiation	否	无		IMR90 cell	E_02_0217	PCR, Western blot, flow cytometry, immunofluorescence staining	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).		Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).	Immunohistochemical staining	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).			PCR,Western blot,Flow cytometry,免疫荧光染色				TNNT2
31518916	chr7	148804819	148806819	EZH2	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.	human,mouse	connective tissue	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	Inflammatory cell	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.		The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.	Immunohistochemical staining	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.			PCR,Western blot,Flow cytometry,免疫荧光染色				EZH2
31518916	chr17	42310415	42312415	STAT3	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I	human,mouse	lung	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	pneumocyte	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I		Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I	Immunohistochemical staining	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I			PCR,Western blot,Flow cytometry,免疫荧光染色				STAT3
31518916	chr17	78354497	78356497	SOCS3	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	human,mouse	Epithelial tissues	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	epithelial cell	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.		In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Immunohistochemical staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.			PCR,Western blot,Flow cytometry,免疫荧光染色				SOCS3
31518916	chr2	190905505	190907505	STAT1	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	human,mouse	Epithelial tissues	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	epithelial cell	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.		In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Immunohistochemical staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.			PCR,Western blot,Flow cytometry,免疫荧光染色				STAT1
31517633	chr19	2246854	2248854	AMH	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).	human,mouse	stomach	High+Lowthroughput	Ulmus minor bark hydro-alcoholic extract ameliorates histological parameters and testosterone level in an experimental model of PCOS rats	否	无	Gastric adenocarcinoma, polycystic ovary syndrome	gastric adenocarcinoma cell	E_02_0219	PCR 	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).		Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).	Immunohistochemical staining	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).			PCR 				AMH
31515577	chr19	4966088	4968088	KDM4B	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	human,mouse	bone	High+Lowthroughput	Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling	否	无	osteoporosis	Bone marrow stromal cell	E_02_0220	PCR,Western blot 	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.		Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Immunohistochemical staining	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.			PCR,Western blot 				KDM4B
31515577	chr17	7831872	7833872	KDM6B	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	human,mouse	bone	High+Lowthroughput	Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling	否	无	osteoporosis	Bone marrow stromal cell	E_02_0220	PCR,Western blot 	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.		Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Immunohistochemical staining	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.			PCR,Western blot 				KDM6B
31515577	chr17	72118259	72120259	SOX9	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].	human,mouse	bone	High+Lowthroughput	Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling	否	无	osteoporosis	ST2 cell	E_02_0220	PCR,Western blot 	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].		KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].	Immunohistochemical staining	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].			PCR,Western blot 				SOX9
31515496	chr16	67559926	67561926	CTCF	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	human	prostate	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	prostate cancer cell	E_01_0278	PCR,Flow cytometry	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	Immunohistochemical staining	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	CTCF		PCR,Flow cytometry	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.			
31515496	chr14	37586728	37588728	FOXA1	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	human	prostate	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	RWPE1 cell	E_01_0278	PCR,Flow cytometry	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	Immunohistochemical staining	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	FOXA1		PCR,Flow cytometry	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.			
31515496	chr12	114667426	114669426	TBX3	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	human	connective tissue	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	cancer cell	E_01_0278	PCR,Flow cytometry	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Immunohistochemical staining	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	TBX3		PCR,Flow cytometry	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.			
31515496	chr1	107053881	107055881	PRMT6	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	human	connective tissue	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	cancer cell	E_01_0278	PCR,Flow cytometry	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.		Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Immunohistochemical staining	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.			PCR,Flow cytometry				PRMT6
31515496	chr15	26540728	26542728	GABRB3	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.	human	Prostate A.H	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	22Rv1 cell	E_01_0278	PCR,Flow cytometry	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.		Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.	Immunohistochemical staining	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.			PCR,Flow cytometry				GABRB3
31514731	chr16	67559877	67561877	CTCF	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	human	blood	High+Lowthroughput	The first enhancer in an enhancer chain safeguards subsequent enhancer-promoter contacts from a distance	是	无	leukemia	K562 cell	E_01_0279	PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Immunohistochemical staining	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	CTCF		PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.			
31513772	chr9	21074265	21076265	IFNB1	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	human	uterus	High+Lowthroughput	The Nuclear Matrix Protein SAFA Surveils Viral RNA and Facilitates Immunity by Activating Antiviral Enhancers and Super-enhancers	否	无	cervical carcinoma	HeLa cell	E_01_0280	PCR, Western blot, flow cytometry, immunofluorescence staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Immunohistochemical staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	IFNB1		PCR,Western blot,Flow cytometry,免疫荧光染色	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).			
31513343	chr17	42310771	42312771	STAT3	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	human,mouse	connective tissue	High+Lowthroughput	Generation of Nanog reporter mice that distinguish pluripotent stem cells from unipotent primordial germ cells	否	无		pluripotent stem cell	E_02_0221	PCR, flow cytometry, immunofluorescence staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.		Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Immunohistochemical staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.			PCR,Flow cytometry,免疫荧光染色				STAT3
31511694	chr21	45491095	45493095	SLC19A1	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.	human,mouse	blood	High+Lowthroughput	SLC19A1 transports immunoreactive cyclic dinucleotides	否	无	leukemia	B cell	E_02_0222	Western blot,PCR,Flow cytometry	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.		SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.	Immunohistochemical staining	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.			Western blot,PCR,Flow cytometry				SLC19A1
31511694	chr17	35868537	35870537	CCL5	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).	human,mouse	blood	High+Lowthroughput	SLC19A1 transports immunoreactive cyclic dinucleotides	否	无	leukemia	THP-1 cells	E_02_0222	Western blot,PCR,Flow cytometry	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).		SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).	Immunohistochemical staining	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).			Western blot,PCR,Flow cytometry				CCL5
31511694	chr19	49656530	49658530	IRF3	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells	human,mouse	blood	High+Lowthroughput	SLC19A1 transports immunoreactive cyclic dinucleotides	否	无	leukemia	L1210 cell	E_02_0222	Western blot,PCR,Flow cytometry	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells		Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells	Immunohistochemical staining	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells			Western blot,PCR,Flow cytometry				IRF3
31511524	chr20	43664495	43666495	MYBL2	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I	human,mouse	connective tissue	High+Lowthroughput	Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes	否	无	Malignancy		E_02_0223	Flow cytometry,Western blot	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I		Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I	Immunohistochemical staining	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I			Flow cytometry,Western blot				MYBL2
31511524	chr12	55964008	55966008	CDK2	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.	human,mouse	kidney	High+Lowthroughput	Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes	否	无	Malignancy	HEK293T	E_02_0223	Flow cytometry,Western blot	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.		High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.	Immunohistochemical staining	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.			Flow cytometry,Western blot				CDK2
31511494	chr7	148804549	148806549	EZH2	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.	mouse	connective tissue	High+Lowthroughput	Interplay of miR-137 and EZH2 contributes to the genome-wide redistribution of H3K27me3 underlying the Pb-induced memory impairment	否	无	Multiple neurodegenerative diseases	PC 12 cell	E_02_0224	PCR, Western blot, immunofluorescence staining	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.		Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.	Immunohistochemical staining	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.			PCR,Western blot,免疫荧光染色				EZH2
31511252	chr5	29675484	29677484	Mnx1	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.	mouse	connective tissue	High+Lowthroughput	Developmentally regulated Shh expression is robust to TAD perturbations	否	无		embryonic stem cell	E_02_0225	PCR,Flow cytometry	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.		Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.	Immunohistochemical staining	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.			PCR,Flow cytometry				Mnx1
31511252	chr16	67559977	67561977	CTCF	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and	mouse	connective tissue	High+Lowthroughput	Developmentally regulated Shh expression is robust to TAD perturbations	否	无		posterior limb bud cell	E_02_0225	PCR,Flow cytometry	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and		Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and	Immunohistochemical staining	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and			PCR,Flow cytometry				CTCF
31509720	chr10	121475640	121477640	FGFR2	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	human	bone	High+Lowthroughput	Genetic Polymorphisms in FGFR2 Underlie Skeletal Malocclusion	是	rs2162540	Osteosarcoma	MG-63 cell	E_01_0281	Western blot,PCR,Flow cytometry	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	Immunohistochemical staining	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	FGFR2		Western blot,PCR,Flow cytometry	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.			
31509720	chr6	45325598	45327598	RUNX2	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	human	bone	High+Lowthroughput	Genetic Polymorphisms in FGFR2 Underlie Skeletal Malocclusion	是	rs11200014	Osteosarcoma	cementoblast	E_01_0281	Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Immunohistochemical staining	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	RUNX2		Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.			
31509720	chr18	51025518	51027518	SMAD4	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	human	lung	High+Lowthroughput	Genetic Polymorphisms in FGFR2 Underlie Skeletal Malocclusion	是	rs2981578	asthma	NHLF cell	E_01_0281	Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Immunohistochemical staining	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	SMAD4		Western blot,PCR,Flow cytometry	That is, rs21625