Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epidermis Kif3a knockout transcriptome reveals genes involved in skin barrier homeostasis

ABSTRACT: In order to address Kif3a role in skin barrier, we performed RNA-seq on 8 week old animals and addressed diffferentially expressed genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE151706 | GEO | 2020/07/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epidermis Kif3a knockout transcriptome reveals genes involved in skin barrier homeostasis

Project description:Epidermis Kif3a knockout transcriptome reveals genes involved in skin barrier homeostasis

| PRJNA637026 | ENA

Conditional keratinocyte-specific ADAM17 knockout in mice alters skin homeostasis

Project description:This study investigates the role of ADAM17 (a disintegrin and metalloproteinase 17) in skin homeostasis. Here, we show that mice lacking ADAM17 in keratinocytes have a normal epidermal barrier and skin architecture at birth, but develop pronounced defects in epidermal barrier integrity soon after birth and chronic dermatitis as adults. The dysregulated expression of epidermal differentiation proteins becomes evident 2 days after birth, followed by transepidermal water loss and inflammatory immune cell infiltration. Our results identify a previously unappreciated critical role of the ADAM17/EGFR signaling axis in maintaining the homeostasis of the postnatal epidermal barrier. The genome-wide effects of ADAM17 deficiency were analyzed using Agilent Whole Mouse Genome microarrays. Conditional keratinocyte-specific ADAM17 knockout mice were generated by crossing Adam17flox/flox mice with keratin-14-Cre (Krt14-Cre) transgenic mice. Adam17flox/+Krt14-Cre mice were mated with Adam17flox/flox mice to generate pups of Adam17flox/flox Krt14-Cre positive (cKO) and Krt14-Cre negative (wild-type) control littermates. The genetic background was a mix of 129Sv and C57BL/6. As material, back skin tissue biopsies (postnatal day 10) from n = 2 wild-type skin and n = 2 ADAM17 epidermal KO skin (matched WT-cKO pairs from two different litters) were used in this study.

2012-06-20 | E-GEOD-38830 | biostudies-arrayexpress

Microbiome dynamics of human epidermis following skin barrier disruption.

Project description:BackgroundRecent advances in sequencing technologies have enabled metagenomic analyses of many human body sites. Several studies have catalogued the composition of bacterial communities of the surface of human skin, mostly under static conditions in healthy volunteers. Skin injury will disturb the cutaneous homeostasis of the host tissue and its commensal microbiota, but the dynamics of this process have not been studied before. Here we analyzed the microbiota of the surface layer and the deeper layers of the stratum corneum of normal skin, and we investigated the dynamics of recolonization of skin microbiota following skin barrier disruption by tape stripping as a model of superficial injury.ResultsWe observed gender differences in microbiota composition and showed that bacteria are not uniformly distributed in the stratum corneum. Phylogenetic distance analysis was employed to follow microbiota development during recolonization of injured skin. Surprisingly, the developing neo-microbiome at day 14 was more similar to that of the deeper stratum corneum layers than to the initial surface microbiome. In addition, we also observed variation in the host response towards superficial injury as assessed by the induction of antimicrobial protein expression in epidermal keratinocytes.ConclusionsWe suggest that the microbiome of the deeper layers, rather than that of the superficial skin layer, may be regarded as the host indigenous microbiome. Characterization of the skin microbiome under dynamic conditions, and the ensuing response of the microbial community and host tissue, will shed further light on the complex interaction between resident bacteria and epidermis.

| S-EPMC3580493 | biostudies-literature

Conditional keratinocyte-specific ADAM17 knockout in mice alters skin homeostasis

2012-06-21 | GSE38830 | GEO

Single cell transcriptomics of human epidermis shows decreased expression of several structural genes associated with skin barrier development in aged skin

Project description:Epidermal keratinocytes are continuously dividing cells which, upon differentiation establish the outer skin barrier, the stratum corneum. In older age the epidermis becomes thinner, papillary protrusions flatten and the capacity for skin barrier repair decreases. Here we performed single-cell RNA sequencing of epidermal keratinocytes obtained by suction blisters from the volar forearm of younger (20-30) and older (65-70) healthy female individuals.

2024-08-28 | GSE275846 | GEO

Development of gene expression signatures for barrier recovery phase in epidermis from acute barrier disruption

Project description:The skin barrier consists of multiple lipid-enriched layers. Sodium lauryl sulfate is a well-known substance that can disrupt the skin barrier. The mechanisms underlying the barrier repair process, especially the influence of topical sodium lauryl sulfate treatment in the barrier recovery phase remain unresolved. To understand the process of reconstruction of the intercellular lipid layer of the skin after acute barrier disruption by sodium lauryl sulfate treatment in vivo.

2023-01-01 | GSE146969 | GEO

Hair follicles modulate skin barrier function

Project description:We generated KA mutant mice (Krt14-CreERT + ABCA12-flox/flox) and controls (ABCA12-flox/flox) that enabled us to assess the effects of deleting a critical barrier gene, ABCA12, in the skin epidermis following tamoxifen treatment. These studies identified numerous differentially expressed genes (DEGs) upon barrier disruption/ABCA12 deletion, including compensatory upregulation of genes involved with epidermal differentiation and barrier function. Overall, this data-set provides a global view of molecular changes that occur in adult mouse skin following barrier perturbation.

2024-05-20 | GSE254889 | GEO

Targeted deletion of Crif1 in mouse epidermis impairs skin homeostasis and hair morphogenesis.

Project description:The epidermis, which consists mainly of keratinocytes, acts as a physical barrier to infections by regulating keratinocyte proliferation and differentiation. Hair follicles undergo continuous cycling to produce new one. Therefore, optimum supply of energy from the mitochondria is essential for maintaining skin homeostasis and hair growth. CRIF1 is a mitochondrial protein that regulates mitoribosome-mediated synthesis and insertion of mitochondrial oxidative phosphorylation polypeptides into the mitochondrial membrane in mammals. Recent studies reveal that conditional knockout (cKO) of Crif1 in specific tissues of mice induced mitochondrial dysfunction. To determine whether the mitochondrial function of keratinocytes affects skin homeostasis and hair morphogenesis, we generated epidermis-specific Crif1 cKO mice. Deletion of Crif1 in epidermis resulted in impaired mitochondrial function and Crif1 cKO mice died within a week. Keratinocyte proliferation and differentiation were markedly inhibited in Crif1 cKO mice. Furthermore, hair follicle morphogenesis of Crif1 cKO mice was disrupted by down-regulation of Wnt/β-catenin signaling. These results demonstrate that mitochondrial function in keratinocytes is essential for maintaining epidermal homeostasis and hair follicle morphogenesis.

| S-EPMC5357846 | biostudies-literature

Hair follicles modulate skin barrier function

Project description:Hair follicles modulate skin barrier function

| PRJNA1072231 | ENA

Microtubule Motor KIF3A Regulates Pulmonary Innate Defenses to Aspergillus and Influenza A Virus

Project description:Susceptibility to respiratory infection, decreased barrier function, impaired epithelial regeneration and enhanced inflammation are likely to contribute to the association between the KIF3A gene and asthma pathogenesis.

2019-09-01 | GSE126323 | 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