Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing from epidermis of LAMA3-deficient mice

ABSTRACT: RNA sequencing from epidermis of LAMA3-deficient mice

PROVIDER: PRJNA609121 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11194375_1.fastq.gz	Fastqsanger.gz
	SRR11194375_2.fastq.gz	Fastqsanger.gz
	SRR11194376_1.fastq.gz	Fastqsanger.gz
	SRR11194376_2.fastq.gz	Fastqsanger.gz
	SRR11194377_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RNA sequencing of Rictor-deficient epidermis

Project description:RNA sequencing of Rictor-deficient epidermis

| PRJNA551008 | ENA

Total RNA sequencing of Skiv2l-deficient mouse epidermis

Project description:Total RNA sequencing of Skiv2l-deficient mouse epidermis

| PRJNA764583 | ENA

RNA sequencing from epidermis of LAMA3-deficient mice

Project description:RNA sequencing data of mouse epidermis isolated from wild type and LAMA3-deficient mice Genetic, clinical and biochemical studies concurred to establish that integrity of the dermal-epidermal junction requires laminin 332, a particular subset of epithelial laminins. Laminin 332 is composed of three subunits, α3, β3 and γ2, encoded by the Lama3, Lamb3 and Lamc2 genes, respectively. In vivo functional analysis of laminin 332 in skin has been prevented because constitutive mutations of any one of the coding genes, either inherited in human or engineered in mice, cause junctional epidermolysis bullosa and early death. Consequently, it is still unknown whether and how laminin 332 contributes to skin homeostasis. To circumvent the problem, we have generated a mouse model in which disruption of the Lama3 gene is conditional and specifically induced in epidermal keratinocytes after birth. It causes a progressive depletion of laminin 332 in the skin of the mouse, which is compatible with life. To assess how laminin 332 supervises epidermal homeostasis, RNA was prepared from keratinocytes isolated from laminin 332-depleted skin and control animals (three each) to compare their gene expression profiles using RNA sequencing.

2021-02-18 | GSE146045 | GEO

Total RNA sequencing of Skiv2l-deficient mouse epidermis

Project description:To identify differentially epxressed RNAs in Skiv2l-deficient mouse epidermis

2022-11-18 | GSE184418 | GEO

Expression data from Integrin-linked kinase (ILK)-deficient epidermis

Project description:ILK is essential for proper development of hair follicles, and for epidermal integrity and repair after injury. To better understand the pathways modulated by ILK in the epidermis, we compared the transcriptomes of ILK-deficient and -expressing epidermis using microarray analyses. Ilktm1Star (with floxed Ilk alleles) and Tg(KRT14-cre)1Amc/J mice were bred, and the resulting mice were bred again with Ilktm1Star mice, to generate animals heterozygos for the KRT14-cre transgene and either heterozygous (ILK-expressing) or homozygous (ILK-deficient) for the floxed Ilk alleles. The epidermis of 3 day-old animals was harvested and used to prepare RNA for the microarrays. The animals used were littermates. RNA from the epidermis of five ILK-deficient and five ILK-expressing mice were used.

2012-01-18 | E-GEOD-35129 | biostudies-arrayexpress

IκBζ-deficient epidermis mediates systemic autoimmune inflammation via skin dysbiosis.

Project description:Skin microbiota affect systemic inflammation through mechanisms that have not been completely elucidated. We previously demonstrated that keratinocyte-specific IκBζ-deficient mice spontaneously develop autoimmune inflammation resembling human Sjögren syndrome. In this study, we examined how IκBζ-deficient epidermis dictates systemic autoimmune inflammation onset. To examine if IκBζ-deficient keratinocytes are susceptible to apoptotic stimuli in a steady state, we performed microarray analysis of untreated murine back epidermis. Data indicate that IκBζ-deficient epidermis is susceptible to environment antigens through apoptosis-related gene upregulation

2022-08-11 | GSE165515 | GEO

RNA-seq analysis comparing Spry1flox/flox mice back epidermis to the back epidermis derived from Spry1 epidermis specific knockout mice

Project description:RNA-seq analysis comparing Spry1flox/flox mice back epidermis to the back epidermis derived from Spry1 epidermis specific knockout mice

| PRJNA974410 | ENA

RNA sequencing of Rictor-deficient epidermis

Project description:We sequenced mRNA from control and Rictor -/- epidermis at E19.5, 3 biological replicates each.

2022-06-25 | GSE133295 | GEO

Hippocampus and hypothalamus RNA-sequencing of WFS1-deficient mice

Project description:Hippocampus and hypothalamus RNA-sequencing of WFS1-deficient mice

| PRJNA398226 | ENA

p107 acts as a tumor suppressor in pRb-deficient epidermis.

Project description:The specific deletion of Rb gene in epidermis leads to altered proliferation and differentiation, but not to the development of spontaneous tumors. Our previous data have demonstrated the existence of a functional compensation of Rb loss by Rbl1 (p107) in as the phenotypic differences with respect to controls are intensified. However, the possible evolution of this aggravated phenotype, in particular in relationship with tumorigenesis, has not been evaluated due to the premature death of the double deficient mice. We have now investigated whether p107 can also act as a tumor suppressor in pRb-deficient epidermis using different experimental approaches. We found spontaneous tumor development in doubly-deficient skin grafts. Moreover, Rb-deficient keratinocytes are susceptible to Ha-ras-induced transformation, and this susceptibility is enhanced by p107 loss. Further functional analyses, including microarray gene expression profiling, indicated that the loss of p107, in the absence of pRb, produces the reduction of p53-dependent pro-apoptotic signals. Overall, our data demonstrate that p107 behaves as a tumor suppressor in epidermis in the absence of pRb and suggest novel tumor-suppressive roles for p107 in the context of functional p53 and activated Ras Keywords: epidermis, tumorigenesis, pRb, p107, Ras, p53, apoptosis

2007-11-13 | GSE9567 | 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