Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of P18 mouse epidermis from K5-FGFR1/FGFR2 knockout and wild-type mice

ABSTRACT: Fibroblast growth factors (FGFs) are master regulators of organogenesis and tissue homeostasis. We generated FGF receptor (FGFR)-deficient mice to unravel their functions in the skin. These mice revealed interesting phenotypic abnormalities, including loss of skin appendages, cutaneous inflammation, keratinocyte hyperproliferation, and acanthosis. To gain insight into the underlying molecular mechanisms, we wanted to identify genes, which are differentially expressed in the skin of wild-type and mutant mice before the onset of phenotypic alterations.

ORGANISM(S): Mus musculus

PROVIDER: GSE111274 | GEO | 2020/06/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Comparison of P18 mouse epidermis from K5-FGFR1/FGFR2 knockout and wild-type mice

Project description:Comparison of P18 mouse epidermis from K5-FGFR1/FGFR2 knockout and wild-type mice

| PRJNA436568 | ENA

Functional analysis of the cytoprotective transcription factor Nrf2 in skin morphogenesis and disease: Identification of Nrf2 target genes

Project description:The Nrf2 transcription factor is a key player in the cellular stress response, which regulates the expression of important antioxidant enzymes and other cytoprotective proteins. We recently generated a novel transgenic mouse model to determine the function of Nrf2 in the skin. These mice revealed interesting phenotypic abnormalities, including hyperkeratosis and acanthosis. To gain insight into the underlying molecular mechanisms, we wanted to identify genes, which are differentially expressed in the skin of wild-type and mutant mice before the onset of phenotypic abnormalities. RNA from whole skin of 3 single P2.5 K5cre-caNrf2 (tg/tg) and 3 single P2.5 K5cre-wt (tg/wt=control) mice were used

2012-02-01 | E-GEOD-35160 | biostudies-arrayexpress

Functional analysis of the cytoprotective transcription factor Nrf2 in skin morphogenesis and disease: Identification of Nrf2 target genes

2012-02-01 | GSE35160 | GEO

Inflammatory mediators suppress FGFR2 expression in human keratinocytes to promote skin inflammation

Project description:FGFs are key orchestrators of development, tissue homeostasis and repair. FGFR deficiency in mouse keratinocytes causes an inflammatory skin phenotype resembling atopic dermatitis (AD). To determine the human relevance of this finding, we generated human keratinocytes with a CRISPR/Cas9-induced knockout of FGFR2. Loss of this receptor promoted the expression of interferon-stimulated genes and other genes involved in inflammation under homeostatic conditions and in particular in response to inflammatory mediators without affecting cell viability. Bioinformatics analyses and functional studies showed strong down-regulation of FGFR2 expression in cultured keratinocytes exposed to various pro-inflammatory stimuli and in keratinocytes of lesional AD skin, which is likely to further aggravate the inflammatory phenotype. These results reveal a key function of FGFR2 in human keratinocytes in the suppression of skin inflammation and suggests a role of FGFR2 down-regulation in AD pathogenesis.

2024-08-29 | GSE267530 | GEO

Expression data from K5-IKKbeta transgenic mouse skin

Project description:IKKbeta is a subunit of the IkB kinase (IKK) complex required for NF-kB activation in response to pro-inflammatory signals. NF-kB regulates the expression of many genes involved in inflammation, immunity and apoptosis, and also controls cell proliferation and differentiation in different tissues; however, its function in skin physiopathology remains controversial. We here report the alterations caused by increased IKKbeta activity in basal cells of the skin of transgenic mice. Transgenic mice which express the IKKbeta gene under the control of the keratin K5 regulatory elements were generated. We analyzed back skins from wildtype and transgenic animals. Each individual array has RNA from three different mice of the same genotype.

2010-03-22 | E-GEOD-17511 | biostudies-arrayexpress

Expression data from K5-IKKbeta transgenic mouse skin

2010-03-22 | GSE17511 | GEO

Analysis of mRNA expression differences in the skin of Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice

Project description:This SuperSeries is composed of the following subset Series: GSE17344: Analysis of spatial mRNA expression differences in the skin of Casp-8F/–K5-Cre or Casp-8F/+K5-Cre mice GSE17345: Analysis of temporal mRNA expression changes in cultured keratinocytes from Casp-8F/–K5-Cre and Casp-8F/+K5-Cre mice Refer to individual Series

2009-07-29 | E-GEOD-17365 | biostudies-arrayexpress

JNK1 Signaling Downstream of the EGFR Pathway Contributes to Imiquimod-induced Skin Inflammation (RNA-seq)

Project description:c-Jun N-terminal protein kinase 1 (JNK1) is involved in multiple biological processes but its implication in inflammatory skin diseases is still poorly defined. Herein, we studied the role of JNK1 in the context of imiquimod-induced skin inflammation. We observed that constitutive ablation of JNK1 reduced imiquimod-induced acanthosis and expression of inflammatory markers. Conditional deletion of JNK1 in myeloid cells led to reduced skin inflammation, a finding that was associated with impaired Aldara®-induced inflammasome activation in vitro. Next, we evaluated the specific role of JNK1 in epidermal cells. We observed a reduced imiquimod-induced acanthosis and keratinocytes proliferation despite similar levels of inflammatory markers. Transcriptomic and epigenomic analysis of keratinocytes revealed the potential involvement of JNK1 in the EGFR signaling pathway. Finally, we show that inhibition of the EGFR pathway reduced imiquimod-induced acanthosis. Taken together, these data indicate that JNK1 plays a dual role in the context of psoriasis by regulating the production of inflammatory cytokines by myeloid cells and the sensitivity of keratinocytes to EGFR ligands. These results suggest that JNK1 could represent a valuable therapeutic target in the context of psoriasis.

2021-01-12 | GSE164580 | GEO

JNK1 Signaling Downstream of the EGFR Pathway Contributes to Imiquimod-induced Skin Inflammation (ATAC-seq)

2021-01-12 | GSE164579 | GEO

Skin graft with dermis and appendages generated in vivo by cell competition

Project description:Autologous skin grafting is a standard treatment for skin defects such as burns. No artificial skin substitutes are functionally equivalent to autologous skin grafts. The cultured epidermis lacks the dermis and does not engraft deep wounds. Although reconstituted skin, which consists of cultured epidermal cells on a synthetic dermal substitute, can engraft deep wounds, it requires the wound bed to be well-vascularized and lacks skin appendages. In this study, we successfully generate complete skin grafts with PSC-derived epidermis with appendages on p63 knockout embryos' dermis. Donor PSC-derived keratinocytes encroach the embryos' dermis by eliminating p63 knockout keratinocytes based on cell-extracellular matrix adhesion mediated cell competition. Although the chimeric skin contains allogenic dermis, it is engraftable as long as autologous grafts. Furthermore, we could generate semi-humanized skin segments by human keratinocytes injection into the amnionic cavity of p63 knockout mice embryos. Niche encroachment opens the possibility of human skin graft production in livestock animals.

2024-02-10 | GSE252023 | 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