Enhancer ID: | E_02_179 | |
Enhancer symbol: | -- | |
Species: | Mouse | |
Position : | chr15:63865799-63896492 |
|
Biosample name: | HCT 116 | |
Experiment class : | Low+High throughput |
Enhancer type: | Super-Enhancer | |
Disease: | Colon Cancer | |
DO: | DOID:219 | |
Mesh: | D003110 | |
Distance from TSS: | >2KB | |
Pubmed ID: | 27941798 |
Enhancer experiment: | ChIP-seq | |
Enhancer experiment description: | To determine if control of enhancer activity by SWI/SNF complexes is coordinated with TFs, we analyzed sequence motifs at enhancers sensitive to ARID1A loss. The CTCF motif was relatively depleted in regions of H3K27ac loss, implying CTCF-bound insulator regions may resist modulation, while the AP1 (JUND/FOSL1) motif was most enriched (Fig. 5a, Supplementary Table 5).Among factors assessed in HCT116 cells, binding of these TFs correlated most strongly with SWI/SNF occupancy (Supplementary Fig. 6b) and was higher at enhancers that lost activity than at enhancers that were unaffected by ARID1A deficiency (Fig. 5c). |
Target gene : | Arid1a(1110030E03Rik,BAF250a,Osa1,Smarcf1) | |
Strong evidence: | -- | |
Less strong evidence: | ChIP-seq,ChIP-qPCR | |
Target gene experiment description: | To determine if control of enhancer activity by SWI/SNF complexes is coordinated with TFs, we analyzed sequence motifs at enhancers sensitive to ARID1A loss. The CTCF motif was relatively depleted in regions of H3K27ac loss, implying CTCF-bound insulator regions may resist modulation, while the AP1 (JUND/FOSL1) motif was most enriched (Fig. 5a, Supplementary Table 5).Among factors assessed in HCT116 cells, binding of these TFs correlated most strongly with SWI/SNF occupancy (Supplementary Fig. 6b) and was higher at enhancers that lost activity than at enhancers that were unaffected by ARID1A deficiency (Fig. 5c). |
TF name : | Arid1a(1110030E03Rik,BAF250a,Osa1,Smarcf1)Arid1b(8030481M12,9330189K18Rik,AI836955,Ardi1b,B230217J03Rik,BAF250B,mKIAA1235) | |
TF experiment: | ChIP-seq | |
TF experiment description: | ChIP-Seq profiles for HCT116 cells, including those generated by ENCODE21 (Encyclopedia of DNA Elements, Supplementary Table 6), revealed further that H3K27ac loss was most strongly associated with sites bound in WT cells by SWI/SNF complexes and/or TFs including AP1, CEBPB, and TEAD4 (Fig. 5b). Among factors assessed in HCT116 cells, binding of these TFs correlated most strongly with SWI/SNF occupancy (Supplementary Fig. 6b) and was higher at enhancers that lost activity than at enhancers that were unaffected by ARID1A deficiency (Fig. 5c) |
Enhancer function : | -- |
Enhancer function experiment: | -- |
Enhancer function experiment description: |
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SNP ID: | -- | |
SNP position: | -- |
SNP experiment: | -- |
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