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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome wide identification of p63 binding sites in human neonatal foreskin keratinocytes

ABSTRACT: We report here genome wide identification of p63 binding sites in cycling neonatal foreskin keratinocytes using high throughput sequencing of ChIP enriched DNA. Analysis of gene ontology, database mining with integration with publicly available data, reveals a role for p63 in transcriptional regulation of multiple genes genetically linked to cleft palate. In addition, we identify AP-2Î±, a transcription factor which, when mutated, also results in craniofacial clefting syndrome, as a co-regulator of p63 responsive genes. Examination of p63 binding sites in neonatal foreskin keratinocytes

ORGANISM(S): Homo sapiens

SUBMITTER: Simon McDade

PROVIDER: E-GEOD-32061 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of p63 binding sites identifies AP-2 factors as co-regulators of epidermal differentiation.

McDade Simon S SS Henry Alexandra E AE Pivato Geraldine P GP Kozarewa Iwanka I Mitsopoulos Constantinos C Fenwick Kerry K Assiotis Ioannis I Hakas Jarle J Zvelebil Marketa M Orr Nicholas N Lord Christopher J CJ Patel Daksha D Ashworth Alan A McCance Dennis J DJ

Nucleic acids research 20120509 15

The p63 transcription factor (TP63) is critical in development, growth and differentiation of stratifying epithelia. This is highlighted by the severity of congenital abnormalities caused by TP63 mutations in humans, the dramatic phenotypes in knockout mice and de-regulation of TP63 expression in neoplasia altering the tumour suppressive roles of the TP53 family. In order to define the normal role played by TP63 and provide the basis for better understanding how this network is perturbed in dise ...[more]

PMID: 22573176

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Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress [ChIP-Seq]

Project description:In response to genotoxic stress the TP53 tumour suppressor activates target gene expression to induce cell cycle arrest or apoptosis depending on the extent of DNA damage. These canonical activities can be repressed by TP63 in normal stratifying epithelia to maintain proliferative capacity or drive proliferation of squamous cell carcinomas, where TP63 is frequently overexpressed/amplified. Here we use ChIP-sequencing, integrated with microarray analysis, to define the genome wide interplay between TP53 and TP63 in response to genotoxic stress in normal cells. We reveal that TP53 and TP63 bind to overlapping, but distinct cistromes of sites through utilization of distinctive consensus motifs and that TP53 is constitutively bound to a number of sites. We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity. Collectively, this results in a global TP53 dependent repression of cell cycle progression, mitosis and DNA damage repair concomitant with activation of anti-proliferative and pro-apoptotic canonical target genes. Further analyses reveals that in the absence of genotoxic stress TP63 plays an important role in maintaining expression of DNA repair genes, loss of which results in defective repair Examination of p63 and p53 binding sites in neonatal foreskin keratinocytes in response to adriamycin or cisplatin treatment

2014-04-11 | E-GEOD-56674 | biostudies-arrayexpress

Genome wide identification of p63 binding sites in human neonatal foreskin keratinocytes

Project description:We report here genome wide identification of p63 binding sites in cycling neonatal foreskin keratinocytes using high throughput sequencing of ChIP enriched DNA. Analysis of gene ontology, database mining with integration with publicly available data, reveals a role for p63 in transcriptional regulation of multiple genes genetically linked to cleft palate. In addition, we identify AP-2Î±, a transcription factor which, when mutated, also results in craniofacial clefting syndrome, as a co-regulator of p63 responsive genes.

2012-06-08 | GSE32061 | GEO

TP63 regulation of epithelial to mesenchymal transition in an experimental prostate cell model

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Genome wide characterization reveals complex interplay between TP53 and TP63 in response to genotoxic stress

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-04-30 | E-GEOD-56640 | biostudies-arrayexpress

Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

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Genome-wide profiling of p63 binding sites identifies genes and regulatory elements for p63-related disorders

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2012-06-18 | E-GEOD-33571 | biostudies-arrayexpress

Transcription factor p63 bookmarks genomic loci in epithelial cells and regulates a subset of target genes during epidermal differentiation through dynamic enhancers (ChIP-Seq)

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Homo sapiens

Project description:Genome wide identification of p63 binding sites in human neonatal foreskin keratinocytes

| PRJNA147615 | ENA

Generation of induced keratinocyte stem cells from human urine cells by defined transcription factors

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2019-04-11 | GSE129316 | GEO

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