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KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity [RNA-seq]

ABSTRACT: KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity [RNA-seq]

PROVIDER: PRJNA989162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25079785_1.fastq.gz	Fastqsanger.gz
	SRR25079785_2.fastq.gz	Fastqsanger.gz
	SRR25079786_1.fastq.gz	Fastqsanger.gz
	SRR25079786_2.fastq.gz	Fastqsanger.gz
	SRR25079787_1.fastq.gz	Fastqsanger.gz

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KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity [ChIP-seq]

Project description:A series of Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) experiments were conducted to investigate the effect and mechanism of KDM5C on the recruitment of BRD4 to chromatin, and the effect of this process on histone modification and gene expression. We then performed ChIP-seq for BRD4, KDM5C, H3K27ac, H3K4me3, and H3K4me1 in HeLa and its derivatives cell lines.

2024-01-17 | GSE236169 | GEO

KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity

Project description:KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity

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KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity [ChIP-seq]

Project description:KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity [ChIP-seq]

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KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity [RNA-seq]

Project description:To investigate the effect of the KDM5C depletion on transcription, we established HeLa cell lines in which KDM5C has been knocked off. To explore the effect of synergistic lethal action of KDM5C PROTAC drug and BETi on transcription, we treated HeLa cells with JQ1, or compound 3b, or in combination.

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KDM5C-mediated BRD4 recruitment is essential for active states of enhancers and BET inhibitor sensitivity

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Hematopoietic transcription factors and p300/CBP shape the effects of BET bromodomain inhibition in leukemia [ChIP-Seq]

Project description:The bromodomain and extraterminal (BET) protein Brd4 is a validated drug target in leukemia, yet its regulatory function in this disease is not well understood. Here, we show that Brd4 chromatin occupancy in acute myeloid leukemia closely correlates with the hematopoietic transcription factors (TFs) Pu.1, Fli1, Erg, C/EBPα, C/EBPβ, and Myb at nucleosome-depleted enhancer and promoter regions. We provide evidence that these TFs, in conjunction with the lysine acetyltransferase activity of p300/CBP, facilitate Brd4 recruitment to their occupied sites to promote transcriptional activation. Moreover, chemical inhibition of BET bromodomains is found to suppress the functional output each hematopoietic TF, thereby interfering with essential lineage-specific transcriptional circuits in this disease. These findings reveal a chromatin-based signaling cascade comprised of hematopoietic TFs, p300/CBP, and Brd4, which supports leukemia maintenance and is suppressed by BET bromodomain inhibition. ChIP-Seq for regulatory factors of Brd4 in MLL-AF9 transformed acute myeloid leukemia cells (RN2)

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BET bromodomain proteins function as master transcription elongation factors independent of CDK9 recruitment [NET-seq]

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