About Enhancer
| Enhancer ID: | E_02_0547 |
| Species: | human |
| Position : | chr21:34785412-34787412   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Myeloid leukemia |
| Pubmed ID: | 29958106 |
| Enhancer experiment: | Flow cytometry, quantitative RT-PCR, RNA SEQ, chip qPCR, chip SEQ, ATAC qPCR, ATAC SEQ, immunoblotting |
| Enhancer experiment description: | The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993). |
About Target gene
| Target gene : | RUNX1(BTEB2,CKLF,IKLF),MYC(MRTLC,bHLHe39,c-Myc),CBFB,MYH11 |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993).;The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993).;The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993).;The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993). |
About TF
| TF name : | -- |
| TF experiment: | ?????,Quantitative RT-PCR,RNA-seq,ChIP qPCR,ChIP-seq,ATAC-qPCR,ATAC-seq,Immunoblotting |
| TF experiment description: | The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993).;The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993).;The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993).;The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993). |
About Function
| Enhancer function : | The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993). |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
The fusion oncoprotein CBF?-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBF?-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression. The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBF?-SMMHC (Liu et al., 1993). |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
| GeneName | Pathway Name | Source | Gene Number |
|---|
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene