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Homo sapiens

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

PROVIDER: PRJNA147615 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR349685.fastq.gz	Fastqsanger.gz
	SRR349686.fastq.gz	Fastqsanger.gz
	SRR349687.fastq.gz	Fastqsanger.gz
	SRR349688.fastq.gz	Fastqsanger.gz

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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. Examination of p63 binding sites in neonatal foreskin keratinocytes

2012-06-07 | E-GEOD-32061 | biostudies-arrayexpress

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

2012-06-08 | GSE32061 | GEO

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

Project description:We identified p63 target genes and binding sites responsible for ectodermal defects by genome-wide profiling of p63 binding using ChIP-seq and expression analysis in human primary keratinocytes from patients with p63 mutations. As proof of principle, we identified a novel de novo microdeletion causing limb defects (SHFM1) that includes a p63 binding site functioning as a cis-regulatory element to control expression of the distally located DLX5/DLX6 genes essential for limb development. Our data demonstrate that target genes and regulatory elements detected in this study can serve as powerful tools to identify causative mutations of unresolved ectodermal disorders. ChIP-seq profiles of p63 in primary human keratinocytes established from two different normal individuals.

2010-08-15 | E-GEOD-17611 | biostudies-arrayexpress

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

Project description:Analysis of induced keratinocyte stem cells from male/female urine cells (MiKSC/FiKSC) by defined transcription factors vs. foreskin derived primary human neonatal epidermal keratinocytes (pKC) and male/female urine cells (MUC/FUC). Results provide insight into molecular similarities between induced keratinocyte stem cells and human foreskin derived primary human neonatal epidermal keratinocytes.

2019-04-11 | GSE129316 | GEO

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

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

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Mutant p63 affects epidermal cell identity through rewiring the enhancer landscape

Project description:<p>Transcription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. Mutations in the p63 DNA-binding domain are associated with Ectrodactyly Ectodermal Dysplasia Cleft Lip/Palate (EEC) syndrome. Underlying molecular mechanism of these mutations however remain unclear. Here we characterized the transcriptome and epigenome of p63 mutant keratinocytes derived from EEC patients. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed an altered enhancer landscape in p63 mutant keratinocytes contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression and the altered enhancer landscape. Our findings identify an unreported disease mechanism whereby mutant p63 rewires the enhancer landscape and affects epidermal cell identity, consolidating the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes.</p>

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Chromatin modification is not a prerequisite for p63 binding but p63 binding can elicit chromatin remodeling

Project description:Transcription factor (TF) p63 is a master regulator playing critical roles in epidermal development and other cellular processes. Our lab’s previous research deciphered a distinct chromatin architecture at p63 bound site in keratinocytes. In order to figure out whether those chromatin modifications already exist before p63 binding, or p63 occupancy contributes to such chromatin marks, we built p63-expressing cell lines. We then obtained p63 bound regions in these overexpressing cell line, and looked at different histone marks at those sites before p63 occupancy. As shown in the results, before p63 binding, the targeting sites have barely detectable histone marks, indicating p63’s capability to approach unmodified chromatins. Moreover, there is no significant difference in chromatin marks between p63 bound sites and unbound sites when no p63 binding happens. Our in vivo findings were confirmed by examining p63 binding to unmodified nucleosomes in vitro, showing that histone modification is not indispensable for p63 binding but binding site positioning on nucleosome does play a role. Overall, our results suggest that histone modifications do not affect p63 binding, and p63 protein can bind to inaccessible, weakly modified chromatin regions in vivo.

2020-12-01 | GSE140329 | GEO

Expression signatures and cytogenetic aberrations in HPV16 E6, E7 and E6/E7-positive immortalized human epithelial cells

Project description:Identification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes Keywords: ordered

2013-11-27 | GSE14051 | GEO

Expression signatures and cytogenetic aberrations in HPV16 E6, E7 and E6/E7-positive immortalized human epithelial cells

Project description:Identification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes Keywords: ordered We used microarrays to identify differentially expressed genes in human foreskin keratinocytes (HFK) transfected with retroviral vectors harboring the human papillomavirus type 16 oncogenes E6, E7, or E6/E7 in comparison to HFK containing the empty vector control pLXSN.

2013-11-27 | E-GEOD-14051 | biostudies-arrayexpress

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