Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Disrupted transcriptional network in ΔNp63 AEC tissue model [ChIP-Seq]

PROVIDER: PRJNA154341 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR363793.fastq.gz	Fastqsanger.gz
	SRR363794.fastq.gz	Fastqsanger.gz
	SRR363795.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

Disrupted transcripitonal network in ΔNp63 AEC tissue model

Project description:This SuperSeries is composed of the following subset Series: GSE33495: Disrupted transcripitonal network in ΔNp63 AEC tissue model [gene expression] GSE33571: Disrupted transcriptional network in ΔNp63 AEC tissue model [ChIP-Seq] Refer to individual Series

2012-06-17 | E-GEOD-33572 | biostudies-arrayexpress

Disrupted transcripitonal network in ΔNp63 AEC tissue model

Project description:Disrupted transcripitonal network in ΔNp63 AEC tissue model

| PRJNA148567 | ENA

Homo sapiens

Project description:Disrupted transcripitonal network in ΔNp63 AEC tissue model [gene expression]

| PRJNA154281 | ENA

Disrupted transcriptional network in ΔNp63 AEC tissue model [ChIP-Seq]

Project description:The transcriptional basis for disrupted epidermal differentiation arising from TP63 AEC mutations remains to be elucidated. Here we present an organotypic model of AEC dysfunction that phenocopies differentiation defects observed in AEC patient skin. Transcriptional analysis of model AEC tissue revealed impaired induction of differentiation regulators, including OVOL1, GRHL3, KLF4, PRDM1 and ZNF750. Genome wide binding analyses of TP63 during epidermal differentiation showed direct binding of OVOL1, GRHL3, and ZNF750 promoters suggesting AEC mutants prevent normal activation of these targets by direct transcriptional interference. Remarkably, exogenous ZNF750 restores impaired epidermal differentiation caused by AEC mutation. Thus, repression of ZNF750 is central to disrupted epidermal differentiation in model AEC tissue. ChIP-Seq analysis: Examination of p63 binding in proliferating and differentiating human keratinocytes

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

Disrupted transcriptional network in ΔNp63 AEC tissue model [ChIP-Seq]

2012-06-18 | GSE33571 | GEO

Disrupted transcripitonal network in ΔNp63 AEC tissue model [gene expression]

2012-06-18 | GSE33495 | GEO

Disrupted transcripitonal network in ΔNp63 AEC tissue model [gene expression]

Project description:The transcriptional basis for disrupted epidermal differentiation arising from TP63 AEC mutations remains to be elucidated. Here we present an organotypic model of AEC dysfunction that phenocopies differentiation defects observed in AEC patient skin. Transcriptional analysis of model AEC tissue revealed impaired induction of differentiation regulators, including OVOL1, GRHL3, KLF4, PRDM1 and ZNF750. Genome wide binding analyses of TP63 during epidermal differentiation showed direct binding of OVOL1, GRHL3, and ZNF750 promoters suggesting AEC mutants prevent normal activation of these targets by direct transcriptional interference. Remarkably, exogenous ZNF750 restores impaired epidermal differentiation caused by AEC mutation. Thus, repression of ZNF750 is central to disrupted epidermal differentiation in model AEC tissue. Gene expression analysis: To establish a differentiation signature for primary human keratinocytes, with p63i-depleted, and ΔNp63α AEC mutants overexpressed, total RNA was isolated in biologic duplicate from cells in different conditions and hybridized to Affymetrix HG-U133 2.0 Plus arrays.

2012-06-17 | E-GEOD-33495 | biostudies-arrayexpress

p63 ChIP-seq analysis comparing WT, TAp63-null, and DNp63-null primary murine keratinocytes

Project description:We performed a ChIP-seq analysis characterizing the p63 binding sites in primary keratinocytes obtained from E18.5 mice of 3 different genotypes (WT, TAp63-/-, and ΔNp63-/-). We aimed to identify the specific genomic regions bound by TAp63 and ΔNp63 in physiological conditions.

2018-03-20 | GSE79448 | GEO

RNA-seq analysis comparing WT, TAp63-null, and DNp63-null primary murine keratinocytes

Project description:We performed an RNA-seq analysis characterizing expression profiles in primary keratinocytes obtained from E18.5 mice of 3 different genotypes (WT, TAp63-/-, and ΔNp63-/-). We aimed to identify the specific transcriptional target genes regulated by TAp63 and ΔNp63 in physiological conditions.

2018-03-20 | GSE79447 | GEO

∆Np63 executes an oncogenic program through the regulation of a common landscape of super-enhancer associated genes in non-small cell lung cancer

Project description:Distinct lung stem cells give rise to lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC). ΔNp63 guides development of these cells through regulation of terminal differentiation; however, its mechanistic role in lung cancer development has remained elusive. We utilized a ΔNp63-specific conditional knockout mouse model and found that ∆Np63 maintains lung ADC and SCC by keeping lung stem cells in quiescence. ChIP-seq analysis of lung basal cells and alveolar type 2 (AT2) cells lacking ∆Np63 revealed a robust loss of activating histone marks at super enhancers of cell identity genes defining a unifying oncogenic role for ∆Np63 in non-small cell lung cancer.

2021-12-23 | GSE131671 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data