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Homo sapiens

ABSTRACT: Genome-wide map of H3K4me3 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

PROVIDER: PRJNA224699 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1016548.fastq.gz	Fastqsanger.gz
	SRR1016549.fastq.gz	Fastqsanger.gz

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Genome-wide map of H3K4me3 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide H3K4me3 binding in human lymphoblastoid cell lines treated with a DNA-damaging chemotherapeutic reagent doxorubicin. ChIP-Seq analysis of H3K4me3 binding sites in human lymphoblastoid cells treated with Doxorubicin or vehicle

2014-11-14 | E-GEOD-51713 | biostudies-arrayexpress

Genome-wide map of H3K4me3 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

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Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

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Project description:Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with doxorubicin

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Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with ionizing radiation

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Project description:Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with nutlin-3

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Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with nutlin-3

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a MDM2 inhibitor nutlin-3 ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with nutlin-3 or vehicle

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Gene expression in human lymphoblastoid cell-line GM12878 in response to doxorubicin treatment

Project description:To determine if induced p53 binding is associated with gene expression in genome-wide. We examined mRNA levels with the Affymetrix Human Exon 1.0 ST platform in human lymphoblastoid GM12878 cells treated with doxorubicin to activate p53. In response to various cellular stresses, the tumor suppressor gene p53 induces activation or repression of more than a thousand human genes. Selective binding and transactivation of a large potential pool of p53 response elements (REs) is believed to regulate the variation in stress response across stress types and between cell types. To elucidate how the human genome is targeted by p53 at the chromatin level, we mapped the genome-wide localization of p53 and H3K4me3 from Doxo-treated human lymphoblastoid cells, and examined the relationships among p53 occupancy, gene expression, H3K4me3, chromatin accessibility (DNase 1 Hypersensitivity, DHS), ENCODE chromatin states, RE sequence specificity and evolutionary conservation.

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