Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of Ovol2-deficent newborn keratinocytes

ABSTRACT: Gene expression analysis of Ovol2-deficent newborn keratinocytes

PROVIDER: PRJNA487344 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7741103_1.fastq.gz	Fastqsanger.gz
	SRR7741103_2.fastq.gz	Fastqsanger.gz
	SRR7741104_1.fastq.gz	Fastqsanger.gz
	SRR7741104_2.fastq.gz	Fastqsanger.gz
	SRR7741105_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Gene expression analysis of Ovol2-deficent newborn keratinocytes

Project description:We report the differential gene expression differences between control and Ovol2-deficent newborn keratinocytes

2018-11-06 | GSE118915 | GEO

Expression data from isolated keratinocytes from mouse skin with or without Ovol1 and Ovol2 expression

Project description:During epithelial tissue morphogenesis, developmental progenitor cells undergo dynamic adhesive and cytoskeletal remodeling to trigger proliferation and migration. Transcriptional mechanisms that restrict such mild form of epithelial plasticity to maintain lineage-restricted differentiation in committed epithelial tissues are poorly understood. Here we report that simultaneous ablation of transcriptional repressor-encoding Ovol1 and Ovol2 results in expansion and blocked terminal differentiation of embryonic epidermal progenitor cells. Conversely, mice overexpressing Ovol2 in their skin epithelia exhibit precocious differentiation accompanied by smaller progenitor cell compartments. We show that Ovol1/2-deficient epidermal cells fail to undertake alpha-catenin–driven actin cytoskeletal reorganization and adhesive maturation, and exhibit changes that resemble epithelial-to-mesenchymal transition (EMT). Remarkably, these alterations as well as defective terminal differentiation are reversed upon depletion of EMT-promoting transcriptional factor Zeb1. Collectively, our findings reveal Ovol-Zeb1-a-catenin sequential repression and highlight novel functions of Ovol as gatekeepers of epithelial adhesion and differentiation by inhibiting progenitor-like traits and epithelial plasticity. Isolated keratinocytes from control, Ovol1 knockout and Ovol1/2 double knockout were physically isolated for RNA extraction and hybridization on Affymetrix microarrays. In order to identify primary changes, we isolated the keratinocytes from mouse skin and allowed them to grow in culture for 2-5 days.

2015-02-14 | E-GEOD-55072 | biostudies-arrayexpress

Expression data from calcium-induced isolated keratinocytes from mouse skin with or without Ovol1 and Ovol2 expression

Project description:During epithelial tissue morphogenesis, developmental progenitor cells undergo dynamic adhesive and cytoskeletal remodeling to trigger proliferation and migration. Transcriptional mechanisms that restrict such mild form of epithelial plasticity to maintain lineage-restricted differentiation in committed epithelial tissues are poorly understood. Here we report that simultaneous ablation of transcriptional repressor-encoding Ovol1 and Ovol2 results in expansion and blocked terminal differentiation of embryonic epidermal progenitor cells. Conversely, mice overexpressing Ovol2 in their skin epithelia exhibit precocious differentiation accompanied by smaller progenitor cell compartments. We show that Ovol1/2-deficient epidermal cells fail to undertake alpha-catenin–driven actin cytoskeletal reorganization and adhesive maturation, and exhibit changes that resemble epithelial-to-mesenchymal transition (EMT). Remarkably, these alterations as well as defective terminal differentiation are reversed upon depletion of EMT-promoting transcriptional factor Zeb1. Collectively, our findings reveal Ovol-Zeb1-a-catenin sequential repression and highlight novel functions of Ovol as gatekeepers of epithelial adhesion and differentiation by inhibiting progenitor-like traits and epithelial plasticity. Isolated keratinocytes from control, Ovol1 knockout and Ovol1/2 double knockout were physically isolated for RNA extraction and hybridization on Affymetrix microarrays. In order to identify differentiation changes, we isolated the keratinocytes from mouse skin and allowed them to grow in culture for 2-5 days, then added calcium and allowed them to grow another 3-5 days.

2015-02-14 | E-GEOD-55071 | biostudies-arrayexpress

ATAC-sequencing data for 923 enhancer deletion newborn mouse keratinocytes

Project description:ATAC-sequencing data for 923 enhancer deletion newborn mouse keratinocytes

| PRJNA667800 | ENA

p38a-dependent gene expression in keratinocytes

Project description:Gene expression in wild-type and p38a-knockout keratinocytes were compared. Keratinocytes were isolated from newborn mice, and left unirradiated (0 h) and irradiated (4 h) with ultraviolet-B (UVB). C57BL/6 wild-type mice, and keratinocyte-specific p38a-knockout mice on a C57BL/6 background were used for isolation of primary keratinocytes.

2014-01-01 | GSE51206 | GEO

The investigation of OVOL2 regulated gene

Project description:To investigate the OVOL2-regulated gene with MCF7 wild-type and knock-out cells.

2021-12-07 | GSE189947 | GEO

ChIP-seq analysis of genome wide Brg1 binding in mouse primary keratinocytes

Project description:We analyzed Brg1 binding genomeiwide in freshly isolated newborn mouse epidermal keratinocytes using ChIP-seq technology Mouse epidermal keratinocytes were isolated form the newborn C57Bl6 mice and Brg1 binding in their chromatin was analyzed using ChIP-seq technology on Hi-Seq 2500 machine

2013-11-01 | E-GEOD-50921 | biostudies-arrayexpress

p38a-dependent gene expression in keratinocytes

2014-01-01 | E-GEOD-51206 | biostudies-arrayexpress

ChIP-seq analysis of genome wide Brg1 binding in mouse primary keratinocytes

Project description:We analyzed Brg1 binding genomeiwide in freshly isolated newborn mouse epidermal keratinocytes using ChIP-seq technology

2013-11-01 | GSE50921 | GEO

Identification of Ovol2 binding regions in HC11 cells

Project description:Epithelial cells possess remarkable plasticity, having the ability to become mesenchymal cells through alterations in adhesion and motility (epithelial-to-mesenchymal transition or EMT). Recent studies suggest that EMT endows differentiated epithelial cells with stem cell traits, posing the interesting question of how epithelial plasticity is properly restricted to ensure epithelial differentiation during tissue morphogenesis. Here we identify zinc-finger transcription factor Ovol2 as a key suppressor of EMT of mammary epithelial cells. Epithelia-specific deletion of Ovol2 completely arrests mammary ductal morphogenesis, and depletes epithelial stem/progenitor cell reservoirs. Further, Ovol2-deficient epithelial cells undergo EMT in vivo to become non-epithelial cell types, and that Ovol2 directly represses key EMT inducers such as Zeb1 and regulates stem/progenitor cell responsiveness to TGF-beta. We also provide evidence for a suppressive role of Ovol2 in breast cancer progression. Our findings underscore the critical importance of exquisitely regulating epithelial plasticity to balance stemness with epithelial differentiation in development and cancer. We report ChIPseq data illustrating Ovol2 genome-wide targets in mouse mammary epithelial cells, suggesting that Ovol2 regulates a plethora of genes associated with the EMT process. Immunoprecipitated samples from HC11 mouse mammary epithelial cells with antibodies against Ovol2 and control IgG respectively were used for ChIP-seq experiments.

2014-03-19 | E-GEOD-53925 | biostudies-arrayexpress

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