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MRNA expression profiling of p63-depleted versus wildtype ME180 cells

ABSTRACT: We investigated the transcriptional effects of p63 binding by analyzing ME180 cells depleted for all p63 isoforms via expression of a small hairpin RNA (shRNA) targeting the p63 oligomerization domain. Keywords: differential expression profiling from transcription factor depletion

ORGANISM(S): Homo sapiens

PROVIDER: GSE5993 | GEO | 2006/12/01

SECONDARY ACCESSION(S): PRJNA97483

REPOSITORIES: GEO

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shRNA human ME180 cells depleted for p63 versus wildtype ME180 cells

Project description:We investigated the transcriptional effects of p63 binding by analyzing ME180 cells depleted for all p63 isoforms via expression of a small hairpin RNA (shRNA) targeting the p63 oligomerization domain. Experiment Overall Design: Data were collected from three biological replicates for p63-depleted and control cells respectively.

2008-06-14 | E-GEOD-5993 | biostudies-arrayexpress

ENCODE: p63ActD & p63_mActD ChIP of retinoic acid-stimulated ME180 cells at 0 h (NCBIv35) - strict analysis parameters

Project description:p63 with and without actinomycin D treatment ChIP from retinoic acid stimulated ME180 Cells at 0 hours using Affymetrix ENCODE tiling chip with NCBI build 35 annotation. p63_ActD and p63_mActD ChIP from retinoic acid stimulated ME180 Cells, 0 hours.

2010-06-05 | E-GEOD-3661 | biostudies-arrayexpress

ENCODE: p63ActD & p63_mActD ChIP of retinoic acid-stimulated ME180 cells at 0 h (NCBIv35) - strict analysis parameters

2005-12-13 | GSE3661 | GEO

Expression data from ME180 cells transfected with siControl and siSGK1

Project description:SGK1 knockdown-induced transcriptional changes in ME180 cells.

2019-06-21 | GSE130449 | GEO

Whole genome mapping of p63 binding sites in ME180 human cervical carcinoma cells

Project description:Using tiled microarrays covering the entire human genome, we identify ~5800 target sites for p63, a homolog of the p53 tumor suppressor essential for stratified epithelial development and implicated in epithelial stem cell maintenance. Keywords: ChIP-chip

2006-12-01 | GSE6132 | GEO

Comparison of gene expression profiles of p63 null skin versus wild type skin

Project description:In the absence of p63 expression, the epidermis fails to commit to stratification, resulting in aborted skin development. In this study, gene expression profiles of E18.5 p63 null and wt skin, were compared in an effort to identify genes that are directly or indirectly regulated by p63. Keywords: Genetically modified mice

2005-12-10 | GSE3108 | GEO

Whole genome mapping of p73 binding sites in ME180 human cervical carcinoma cells

Project description:Using chromatin immunoprecipitation and high-resolution tiling arrays covering the human genome, we render a genome-wide map of p73 DNA binding sites in ME180 human cervical carcinoma cells.

2010-09-10 | GSE18650 | GEO

Microarray analysis of palatal shelves from wild-type versus p63-null mouse embryos

Project description:Mutations in the transcription factor p63 underlie of a series of human malformation syndromes which are defined by a combination of epidermal, limb and craniofacial abnormalities including cleft lip and palate. Transcription profiling was performed to determine the role of p63 in vivo mouse palatal shelves. Microarray analysis was done of palatal shelves dissected from E14.0 wild-type versus p63-null mouse embryos.

2017-06-12 | E-MTAB-3145 | biostudies-arrayexpress

Identification of HTRA4 as a trasncritpional target of P63 in trophoblast

Project description:The placenta plays a crucial role in pregnancy success. deltaNp63alpha (p63), a transcription factor from the TP53 family, is highly expressed in villous cytotrophoblasts (CTBs), the epithelial stem cells of the human placenta, and has been shown to be involved in CTB maintenance and differentiation. In this study, we set out to identify mechanism(s) of action of p63, by identifying its downstream targets. We evaluate gene expression changes following overexpression and knockdown of p63 in the JEG3 choriocarcinoma cell line, using microarray-based RNA profiling. We identify High temperature requirement A4 (HTRA4), a placenta-specific serine protease involved in trophoblast differentiation and altered in preeclampsia, as a gene reciprocally regulated by p63, and characterize its expression in primary human placental tissues by RNAseq (PMID 34540826; GSE173372) and in situ hybridization. Forced overexpression of deltaNp63alpha in JEG-3 was obtained by pCMV lentiviral vector infection (empty vector used as control). ) The pLKO.1-based non-targeting scramble and p63-specific short hairpin (shRNA) lentiviral plasmids were used for gene knock-down. Vectors were previously described in Li et al Am J Pathol. 2014 PMID: 25307348.

2024-03-27 | GSE251742 | GEO

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

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