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ChIP-Seq of H4K5acK8ac, H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K9me3, H3K27me3 and BRD2 in H23 NSCLC cell line

ABSTRACT: ChIP-Seq of H4K5acK8ac, H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K9me3, H3K27me3 and BRD2 in H23 NSCLC cell line

PROVIDER: PRJNA412811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6124070.fastq.gz	Fastqsanger.gz
	SRR6124080.fastq.gz	Fastqsanger.gz
	SRR6124071.fastq.gz	Fastqsanger.gz
	SRR6124081.fastq.gz	Fastqsanger.gz
	SRR6124072.fastq.gz	Fastqsanger.gz

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ChIP-Seq of H4K5acK8ac, H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K9me3, H3K27me3 and BRD2 in H23 NSCLC cell line

Project description:The bromodomain and extra-terminal domain (BET) proteins are known as drug targets in diseases. However, the BET protein association profile to histone H4 hyperacetylation is not well understood and BET inhibition effects have been studied more in the context of BRD4 than BRD2. Here, by integrating chromatin and transcriptome analyses of ChIP-seq and Cap Analysis Gene Expression (CAGE) datasets, we show that di-acetylation at K5 and K8 of histone H4 (H4K5acK8ac) co-localizes with H3K27ac and BRD2 in the majority of active enhancers and promoters, where BRD2 has a stronger association with H4K5acK8ac than H3K27ac. Interestingly, although BET inhibition by JQ1 led to complete reduction of BRD2 binding, only local changes of H4K5acK8ac were observed and surprisingly a remarkable number of BRD2-bound genes including MYC and its target genes were upregulated. Using BRD2-enriched sites and transcriptional activity analysis, we identified candidate transcription factors (TFs) potentially involved in the JQ1 response in BRD2-dependent and independent manner.

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ChIP-Seq of H4K5acK8ac and BRD2 in H23 NSCLC cell line treated with 500 nM JQ1 for 24h

Project description:Changes in acetylation of histone H4 are a common hallmark of cancer cells. In leukemia cells, histone H4 is characterized by loss of K16 mono-acetylation. Bromodomain proteins specifically recognize acetylated lysines and have been used as a target for anti cancer drug, JQ1 and iBET. Although acetylation and de-acetylation of histone H4 have been shown to have big impact in cancer cells, little attention has been focused on histone H4-acetylation at a genome level. To uncover potential epigenetic role of hyper-acetylated histone H4 at a genome-wide level in cancer cell, we generated a novel monoclonal antibody specifically recognizing histone H4 with at least two acetylated lysine residues (H4K5ac+K8ac). At the genome-wide level, hyper-acetylated histone H4 is associated with promoter and regulatory element (active enhancer, eRNA and super enhancer). We show that diacetylation at K5 and K8 of histone H4 co-localizes H3K27ac and BRD2 in the majority of active enhancer and promoters. However BRD2 has a stronger association with H4K5acK8ac. Furthermore we identified two specific chromatin states, which separately contain either H3K27ac or acetylated histone H4. Although JQ1 led to global reduction of BRD2 binding on the chromatin, only local changes of histone H4 multi-acetylation were observed upon BET inhibition by JQ1

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ChIP-Seq of H4K5acK8ac and BRD2 in H23 NSCLC cell line treated with 500 nM JQ1 for 24h

Project description:ChIP-Seq of H4K5acK8ac and BRD2 in H23 NSCLC cell line treated with 500 nM JQ1 for 24h

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Project description:We profiled transcriptomes in human lung cancer cell lines H23 and A549 cells.

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CUT&Tag on H3K4me3, H3K27ac, H3K4me1, H3K9me3, H3K27me3, H3K36me3 and H2AK119ub in TX1072 XXΔXic and XO mESCs during differentiation

Project description:CUT&Tag on H3K4me3, H3K27ac, H3K4me1, H3K9me3, H3K27me3, H3K36me3 and H2AK119ub in TX1072 XXΔXic and XO mESCs during differentiation

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Streptomyces sp. H23

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