About Enhancer

Enhancer ID: E_01_279
Enhancer symbol: --
Species: Human
Position : chr7:129854050-129895632
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).

About Target gene

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).

About TF

TF name : --
TF experiment: --
TF experiment description: --

About Function

Enhancer function : --
Enhancer function experiment: --
Enhancer function
experiment description:
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About SNP

SNP ID: --
SNP position: --
SNP experiment: --

Enhancer associated network

The number on yellow line represents the distance between enhancer and target gene

Expression of target genes for the enhancer


Enhancer associated SNPs