Enhancer ID: | E_01_279 | |
Enhancer symbol: | -- | |
Species: | Human | |
Position : | chr7:129854050-129895632 |
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Biosample name: | Adipose Progenitor Cell | |
Experiment class : | Low+High throughput |
Enhancer type: | Enhancer | |
Disease: | -- | |
DO: | -- | |
Mesh: | -- | |
Distance from TSS: | >2KB | |
Pubmed ID: | 28751304 |
Enhancer experiment: | ChIP-seq,FISH | |
Enhancer experiment description: | We also searched for putative MIR335 short- and long-range Enhancers:to this end, we combined chromatin state modeling data from ENC ODE ChIP-seq experiments showing enrichment in H3K4me1 and/or H3K27ac, histone modifications found on inactive and active Enhancers, respectively (Fig. S5 A), with ENCODE genome-wide chromosome conformation capture of Hi-C data (Rao et al., 2014). The Hi-C data reveal multiple pairwise interactions of these predicted enhancers with the MIR335 promoter (Fig. S5, B–D), providing six MIR335-predicted distal enhancer sites (regions r6–r11; Fig. S5 D). Acetylation of H3K27 on MIR335 enhancers detected in ASCLMNA(R482W) after adipogenic induction suggests interac-tions with the MIR335 promoter by chromatin looping (Zhang et al., 2013). We tested this hypothesis by two-color FISH using distinctly labeled promoter and enhancer probes. Probes were generated to cover the MIR335 gene and promoter as well as the distal enhancer element r11 located ∼200 kb upstream of MIR335. In both undifferentiated and differentiated ASCs that were either native or expressing WT LMNA, these promoter and enhancer elements displayed a relatively low incidence of colocalization on the majority of alleles (∼80%; Fig. 6, C and D). After induction of differentiation, however, this proportion markedly increased to 56% of alleles in the LMNA(R482W) mutants, reflecting interaction of a high proportion of MIR335 promoter and enhancer sites (Fig. 6, C and D). |
Target gene : | MIR335(MIRN335,hsa-mir-335,miRNA335,mir-335) | |
Strong evidence: | -- | |
Less strong evidence: | ChIP-seq,FISH | |
Target gene experiment description: | We also searched for putative MIR335 short- and long-range Enhancers:to this end, we combined chromatin state modeling data from ENC ODE ChIP-seq experiments showing enrichment in H3K4me1 and/or H3K27ac, histone modifications found on inactive and active Enhancers, respectively (Fig. S5 A), with ENCODE genome-wide chromosome conformation capture of Hi-C data (Rao et al., 2014). The Hi-C data reveal multiple pairwise interactions of these predicted enhancers with the MIR335 promoter (Fig. S5, B–D), providing six MIR335-predicted distal enhancer sites (regions r6–r11; Fig. S5 D). Acetylation of H3K27 on MIR335 enhancers detected in ASCLMNA(R482W) after adipogenic induction suggests interac-tions with the MIR335 promoter by chromatin looping (Zhang et al., 2013). We tested this hypothesis by two-color FISH using distinctly labeled promoter and enhancer probes. Probes were generated to cover the MIR335 gene and promoter as well as the distal enhancer element r11 located ∼200 kb upstream of MIR335. In both undifferentiated and differentiated ASCs that were either native or expressing WT LMNA, these promoter and enhancer elements displayed a relatively low incidence of colocalization on the majority of alleles (∼80%; Fig. 6, C and D). After induction of differentiation, however, this proportion markedly increased to 56% of alleles in the LMNA(R482W) mutants, reflecting interaction of a high proportion of MIR335 promoter and enhancer sites (Fig. 6, C and D). |
TF name : | -- | |
TF experiment: | -- | |
TF experiment description: | -- |
Enhancer function : | -- |
Enhancer function experiment: | -- |
Enhancer function experiment description: |
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SNP ID: | -- | |
SNP position: | -- |
SNP experiment: | -- |
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