ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively. Overall design: CHL-1 cells were treated with BAY 1238097 or OTX-015, potent and selective Bromodomain and extra terminal domain (BET) inhibitors, before chromatin immunoprecipitation using antibodies directed against BRD4 and acetylated H3K27.

溴结构域和额外末端结构域（Bromodomain and extra terminal domain, BET）抑制剂可降低BET家族蛋白在启动子与增强子位点的结合占据水平，最终引发全基因组范围内的基因转录改变。本研究采用染色质免疫沉淀测序（ChIP-seq）分析，探究由BET抑制剂BAY 1238097与OTX-015分别诱导的启动子与增强子位点结合占据水平的全基因组变化。实验设计：将CHL-1细胞经强效且具有选择性的BET抑制剂BAY 1238097或OTX-015处理后，使用针对BRD4与乙酰化H3K27的抗体开展染色质免疫沉淀实验。