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Genome-wide profiling of H3K27ac (ChIP-seq) in IMR90 cells

ABSTRACT: Genome-wide profiling of H3K27ac (ChIP-seq) in IMR90 cells

PROVIDER: PRJEB18688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1766286.fastq.gz	Fastqsanger.gz
	ERR1766287.fastq.gz	Fastqsanger.gz
	ERR1766288.fastq.gz	Fastqsanger.gz
	ERR1766289.fastq.gz	Fastqsanger.gz

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Genome-wide profiling of H3K27ac (ChIP-seq) in IMR90 cells

Project description:To determine the genome-wide pattern of H3K27ac in IMR90 (ATCC CCL-186) cells we performed ChIP-seq upon hormone treatment (1.5 h, 1 M dexamethasone).

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ChIP-seq for CTCF, H3K4me3 and H3K27ac following CTCF RNAi in LNCaP cells and IMR90 cells

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Project description:Upregulation of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and its associated histone H3 lysine 27 (H3K27) trimethylation frequently occur in human cancer, yet both preclinical and clinical evidence suggested the very limited benefit of EZH2-targeted therapies. This study investigated the underlying mechanisms from a perspective of EZH2 inhibition-caused histone modification crosstalk. A mass spectrometry approach enabled us discovering the alteration of global histone modifications responding to EZH2 inhibition. Feedback upregulation of H3K27 acetylation (H3K27ac) level is closely associated with limited drug response to EZH2 inhibition across multiple cancer types. H3K27ac alteration caused transcriptional activation of oncoproteins confers drug resistant to EZH2 inhibition. Here we used ChIP-Seq analysis to identify the alteration of genome-wide H3K27ac bingding sites with EZH2 inhibitor treatment in human cancer cell lines.

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Genome-wide maps of H3K27ac localization in HUVECs

Project description:H3K27Ac is one of the expressed enhancer markers in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for H3K27ac, and performed ChIP-seq to identify H3K27ac binding site in whole genome manner under hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without hypoxia (1%O2) for 24hours, then H3K27ac binding regions were identified. Normoxia was used as a control condition. HUVECs were used within the first 6 passages.

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