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ShRNA human ME180 cells depleted for p63 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. Experiment Overall Design: Data were collected from three biological replicates for p63-depleted and control cells respectively.

ORGANISM(S): Homo sapiens

SUBMITTER: Annie Yang

PROVIDER: E-GEOD-5993 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Relationships between p63 binding, DNA sequence, transcription activity, and biological function in human cells.

Yang Annie A Zhu Zhou Z Kapranov Philipp P McKeon Frank F Church George M GM Gingeras Thomas R TR Struhl Kevin K

Molecular cell 20061101 4

Using tiled microarrays covering the entire human genome, we identify approximately 5800 target sites for p63, a p53 homolog essential for stratified epithelial development. p63 targets are enriched for genes involved in cell adhesion, proliferation, death, and signaling pathways. The quality of the derived DNA sequence motif for p63 targets correlates with binding strength binding in vivo, but only a small minority of motifs in the genome is bound by p63. Conversely, many p63 targets have motif ...[more]

PMID: 17188034

Similar Datasets

mRNA expression profiling of p63-depleted 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. Keywords: differential expression profiling from transcription factor depletion

2006-12-01 | GSE5993 | GEO

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

Generation of patient-relevant p63 gene signature to identify novel oncogenes and tumor suppressors that contribute to HNSCC development and progression

Project description:To identify novel targets of p63 as part of a patient-centric meta analysis, we performed RNA-sequencing on control and p63-depleted cancer cells (A253 and SCC25). In addition, we performed ChIP-sequencing analysis using multiple p63-specific antibodies, as well as antibodies targeting specific histone modifications(H3K27ac,H3K4me3 and H3K4me1) to evaluate mechanism(s) by which p63 regulates these novel targets. Our analysis identified known and novel oncogenic factors that influence various aspects of cancer development and progression.

2023-07-10 | GSE212752 | GEO

Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231 p63 ChIP-SEQ on MCFDCIS and MDA-MB-231 cell lines

2016-08-11 | E-GEOD-72009 | biostudies-arrayexpress

ChIP-seq of p63 and RNA-seq of knockdown and overexpression of p63

Project description:We performed ChIP-seq of p63 in ME-180 cell line and RNA-seq of knockdown and overexpression of p63

2019-08-06 | GSE135257 | GEO

Identification of p63 binding regions in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS.

Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231

2016-08-11 | GSE72009 | GEO

iTRAQ-based quantitative proteomic analysis of nuclear proteome in VPS35-depleted HeLa cells

Project description:Stable VPS35 knockdown HeLa cells were generated using lentiviral short hairpin RNA (shRNA) construct. Isobaric tags for relative and absolute quantitation (iTRAQ)-based mass spectrometry was used to measure the changes of nuclear protein abundance in VPS35-depleted HeLa cells.

2022-08-12 | PXD027166 | Pride

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

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

2010-08-15 | GSE17611 | GEO