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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Xuting Wang

PROVIDER: E-GEOD-46992 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A polymorphic p53 response element in KIT ligand influences cancer risk and has undergone natural selection.

Zeron-Medina Jorge J Wang Xuting X Repapi Emmanouela E Campbell Michelle R MR Su Dan D Castro-Giner Francesc F Davies Benjamin B Peterse Elisabeth F P EF Sacilotto Natalia N Walker Graeme J GJ Terzian Tamara T Tomlinson Ian P IP Box Neil F NF Meinshausen Nicolai N De Val Sarah S Bell Douglas A DA Bond Gareth L GL

Cell 20131001 2

The ability of p53 to regulate transcription is crucial for tumor suppression and implies that inherited polymorphisms in functional p53-binding sites could influence cancer. Here, we identify a polymorphic p53 responsive element and demonstrate its influence on cancer risk using genome-wide data sets of cancer susceptibility loci, genetic variation, p53 occupancy, and p53-binding sites. We uncover a single-nucleotide polymorphism (SNP) in a functional p53-binding site and establish its influenc ...[more]

PMID: 24120139

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

2013-10-23 | GSE46992 | GEO

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2014-05-21 | E-GEOD-43596 | biostudies-arrayexpress

ChipSeq of conditional knock-in mouse carrying the R178E (EE) mutation in exon 5 of the endogenous mouse Trp53 gene locus.

Project description:The mouse R178E (EE) mutation of the Trp53 is a p53 mutant protein with native conformation that lacks the ability to form tetramers and thus constitutes a mutant form of p53 that lacks DNA binding cooperativity. Here we want to assess DNA binding ability of the EE mutant in MEFs under untreated conditions and following p53 stabilization with the Mdm2 inhibitor nutlin-3a and compare it to p53 KO and WT mice.

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