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

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

PROVIDER: PRJNA989164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25074100_1.fastq.gz	Fastqsanger.gz
	SRR25074100_2.fastq.gz	Fastqsanger.gz
	SRR25074101_1.fastq.gz	Fastqsanger.gz
	SRR25074101_2.fastq.gz	Fastqsanger.gz
	SRR25074105_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 [RNA-seq]

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

| PRJNA989162 | ENA

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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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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Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

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The Kdm5c histone demethylase controls enhancer and promoter function.

Project description:Here, we show that the Kdm5c/Smcx member of the Jarid1 family of H3K4 demethylases is recruited to both enhancer and core promoter elements in ES and neuronal progenitor cells (NPC). Knockdown of Kdm5c deregulates transcription via a local increase in H3K4me3. While at core promoters the function of Kdm5c is to restrict transcription, loss of Kdm5c impairs enhancer function. Remarkably, an impaired enhancer function activates promoter activity from Kdm5c-bound intergenic regions. Our results demonstrate that the Kdm5c demethylase plays a crucial role in the functional identity and discrimination of enhancers and core promoters. We speculate that this is related to recruitment of H3K4me3 binders like the TFIID and NURF complexes6-8. Providing functional identity to genomic regions through balancing enzymes that deposit and remove histone modifications may prove to be a general epigenetic mechanism for the functional indexing of eukaryotic genomes. Examination of the KDM5C binding sites in mouse embryonic stem cells and in neuronal progenitor cells. Effect of KDM5C knock down on H3K4me3 and H3K4me1 levels and gene expression.

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Project description:Cancer arises from the malignant interplay between oncogenic signaling and cell specification. Transcriptionally activated stem, growth and survival programs reshape an epigenomic identity defined by a transcriptional core regulatory circuitry. To study and disrupt oncogenic transcription, we first created inhibitors of BET bromodomains. Selective antagonism of oncogenic transcriptional signaling arises from bromodomain-specific activity. Recently, we innovated a strategy to induce selective and pronounced degradation of BET coactivator proteins via phthalimide conjugation for E3 ubiquitin ligase recruitment. Degraders of BET bromdomains (dBETs) exhibited superior efficacy to bromodomain inhibitors in cultivated leukemia cells, through unknown mechanisms. Here, we use chemically optimized small-molecule degronimids and kinetic measures of chromatin structure and function to unveil an unrecognized, essential role for BRD4 in the control of global productive transcriptional elongation. Rapid loss of BRD4 attenuates phosphorylation of the carboxy-terminal domain of RNA polymerase II, independent of genomewide recruitment of CDK9 to promoters, leading to a collapse of the transcriptional core regulatory circuitry. These mechanistic studies are performed in translational models of T-cell acute lymphoblastic leukemia, a disease emblematic for transcriptional addiction, to establish a rationale for human clinical investigation.

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

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