Enhancer ID: | E_02_189 | |
Enhancer symbol: | -- | |
Species: | Mouse | |
Position : | chr4:97123309-97712957 |
|
Biosample name: | Embryonic Fibroblast | |
Experiment class : | Low+High throughput |
Enhancer type: | Enhancer | |
Disease: | Malignancies | |
DO: | -- | |
Mesh: | -- | |
Distance from TSS: | >2KB | |
Pubmed ID: | 28262751 |
Enhancer experiment: | ChIP-seq | |
Enhancer experiment description: | Following inactivation of either Smarcb1 or Smarca4, we observed little change in H3K27ac levels at promoters, but a marked reduction at many enhancers (Fig. 1b,c). This reduction at enhancers was robust and consistent across replicate experiments performed on MEFs derived from independent mice (Methods, Supplementary Figs 3-7). |
Target gene : | Nfia(1110047K16Rik,9430022M17Rik,CTF,NF1-A,NF1A) | |
Strong evidence: | -- | |
Less strong evidence: | ChIP-seq,Western blot | |
Target gene experiment description: | To investigate whether SWI/SNF is acting directly at active enhancers, we performed ChIP-Seq for the core SWI/SNF subunits SMARCC1 and SMARCA4 in wild-type and Smarcb1-deficient cells. Because the genome-wide binding profiles of these two subunits were very similar (Supplementary Fig. 3), we considered the average of the two experiments to be representative of SWI/SNF binding for each condition. Interestingly, we found that SWI/SNF was bound at the vast majority of enhancers in wild-type cells-over 95% of enhancers showed enrichment (IP>input; Fig. 2a and Supplementary Fig. 9a). Deletion of the Smarcb1 subunit led to a widespread reduction in SWI/SNF binding (Fig. 2b and Supplementary Fig. 9b).Taken together, the targeting of SWI/SNF to enhancers and the association between loss of SWI/SNF binding and the loss of H3K27ac suggests a direct role for the SWI/SNF complex in regulating the enhancer chromatin landscape in MEFs. |
TF name : | Ep300(KAT3B,MKHK2,RSTS2,p300) | |
TF experiment: | ChIP-seq | |
TF experiment description: | To further evaluate how the interaction between SWI/SNF and p300 regulates H3K27ac levels, we immunoprecipitated SWI/SNF complexes using an antibody against the core subunit SMARCC1 and measured histone acetylation activity using recombinant histones as a substrate. With immunoprecipitated SWI/SNF complexes from a RT cell line that lacked SMARCB1, the sample lacked acetyltransferase activity. However, re-expression of SMARCB1 increased H3K27-specific acetyltransferase activity, despite acetylation of H3K9ac being not significantly changed, suggesting the presence of H3K27-specific acetylation activity (Fig. 3d). |
Enhancer function : | -- |
Enhancer function experiment: | -- |
Enhancer function experiment description: |
-- |
SNP ID: | -- | |
SNP position: | -- |
SNP experiment: | -- |
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