Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq II]. Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq II]

The circadian transcription factor Bmal1 accelerates melanoma tumorigenesis through initial cell state dependent mechanisms in which Hif1??, Sox9 or Myh9, MRTF-SRF, AP-1 are involved and modulate tumor microenvironment to favor tumor growth Overall design: CHIP-seq of H3K27ac in cells of different Bmal1 and H3K27ac and H3K4me3 of different Myh9 status

昼夜节律转录因子Bmal1可通过依赖于初始细胞状态的机制加速黑色素瘤的肿瘤发生，该机制涉及缺氧诱导因子1α（HIF1α）、Sox9、Myh9、心肌素相关转录因子-血清反应因子（MRTF-SRF）以及激活蛋白1（AP-1），并可调控肿瘤微环境以促进肿瘤生长。实验整体设计：对不同Bmal1状态下细胞的组蛋白H3赖氨酸27乙酰化（H3K27ac）进行染色质免疫共沉淀测序（ChIP-seq），并对不同Myh9状态下细胞的H3K27ac及组蛋白H3赖氨酸4三甲基化（H3K4me3）进行染色质免疫共沉淀测序。