Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mixture of skin bacteria

ABSTRACT: Microbiome Profiling of mice skin - WT vs HCA2-KO mice

PROVIDER: PRJNA836734 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19153300_1.fastq.gz	Fastqsanger.gz
	SRR19153300_2.fastq.gz	Fastqsanger.gz
	SRR19153301_1.fastq.gz	Fastqsanger.gz
	SRR19153301_2.fastq.gz	Fastqsanger.gz
	SRR19153302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

RNAseq E16.5 mouse skin Irf6 KO vs WT

Project description:RNAseq E16.5 mouse skin Irf6 KO vs WT

| PRJNA510612 | ENA

TAILS on mouse skin deficient for ADAMTS2 and ADAMTS14

Project description:TAILS 4-Plex on mouse skin. 114 - WT; 115 - ADAMTS2-KO; 116 - ADAMTS14-KO; 117 - ADAMTS2TS14-double KO.

2021-04-16 | PXD022179 | Pride

Atrial AMP-activated protein kinase is critical to prevent dysregulation of electrical excitability and atrial fibrillation

Project description:Transcriptional profiling to assess atrial gene expression in atrial LKB1 KO vs. AMPK KO vs. WT mice.

2022-04-05 | GSE200144 | GEO

RNA-seq of skin tissues from WT and Cd1d KO B6 mice

Project description:To investigate the effect of iNKT deficiency in the skin, the analysis of global gene expression in the skin tissues from WT and Cd1d KO mice were performed using RNA-seq data obtained from these samples.

2022-11-06 | GSE205602 | GEO

The aryl hydrocarbon receptor in keratinocytes is essential for murine skin barrier integrity

Project description:The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved in adaptive cell functions, and highly active in the epidermis. AhR-ligands can accelerate keratinocyte differentiation, but a precise role for AhR in the skin barrier is unknown. We here show that transepidermal water loss (TEWL), a parameter of skin barrier integrity, is high in AhR-deficient (AhR-KO) mice. Experiments with conditionally AhR-deficient mouse lines identified keratinocytes as the major responsible cell population for high TEWL. Electron microscopy showed weaker inter-cellular connectivity in the epidermis of keratinocytes in AhR-KO mice, and gene expression analysis identified many barrier-associated genes as AhR targets. Moreover, AhR-deficient mice had higher inter-individual differences in their microbiome. Interestingly, removing AhR-ligands from the diet of wild-type mice mimicked AhR-deficiency regarding the impaired barrier. Vice versa, re-addition of the plant-derived ligand indole-3-carbinol (I3C) rescued the barrier deficiency even in aged mice. Our results suggest that functional AhR expression is critical for skin barrier integrity and that AhR represents a molecular target for the development of novel therapeutic approaches for skin barrier diseases, including dietary intervention.

2016-08-31 | GSE80273 | GEO

Comparing the difference in gene expression between TDAG51 WT vs TDAG51 KO, and TDAG51 KO Tg vs TDAG51 KO

Project description:Transcriptional profiling of postpartum day 0 mouse brain, comparing TDAG51 wild-type (WT) vs TDAG51 knockout (KO), and TDAG51 KO transgenic (Tg) vs TDAG51 KO.

2019-08-17 | GSE118675 | GEO

Facial Skin Biophysical Multi-Parameter and Microbiome-Based Korean Skin Cutoype (KSC) Determination

Project description:In this study, we conducted an integrated analysis of skin measurements, clinical BSTI surveys, and the skin microbiome of 950 Korean subjects to examine the ideal skin microbiome-biophysical association. By utilizing four skin biophysical parameters, we identified four distinct Korean Skin Cutotypes (KSCs) and categorized the subjects into three aging groups based on their age distribution. We established strong connections between 15 core genera and the four KSC types within the three aging groups, revealing three prominent clusters of the facial skin microbiome. Together with skin microbiome variations, skin tone/elasticity distinguishes aging groups while oiliness/hydration distinguishes individual differences within aging groups. Our study provides prospective reality data for customized skin care based on the microbiome environment of each skin type.

| EGAS00001007334 | EGA

The Skin Microbiome of Mycosis fungoides

Project description:The skin Microbiome stratifies Patients with CTCL into two subgroups. One subgroup has a balanced microbiome, while the other subgroups has a skin dybiosis with S. aureus outgrow. This is accompanied by impaired TCR repertoir and poor clinical outcome.

2023-12-01 | GSE221149 | GEO

Modulatory role of skin microbiome against UV

Project description:The role of the skin microbiome in UV-induced immune suppression has been overlooked. We addressed the question of microbial involvement in UV-induced immune suppression by using the standard model of contact hypersensitivity in the presence or absence of the microbiome (in germ-free [GF] and disinfected mice) and found that the microbiome inhibits UV-induced immune suppression. Furthermore, our transcriptome analysis (24 hours after irradiation) showed differential regulation of many genes in the presence or absence of the microbiome, including a predominance of pro-inflammatory cytokines versus immunosuppressive cytokines

2019-05-26 | GSE117359 | GEO

LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [BMDM]

Project description:Patients with cutaneous T cell lymphoma (CTCL) experience high morbidity and mortality due to S. aureus skin infections and sepsis, but the causative immune defect is unclear. We propose that high levels of LAIR2 in CTCL suppress LAIR1 inhibitory signaling, promoting inflammation and tissue damage, which increases S. aureus susceptibility. Mice do not have a LAIR2 homolog, so we used Lair1 KO mice to model LAIR2 overexpression. In a model of subcutaneous S. aureus skin infection, Lair1 KO mice had significantly larger abscesses and areas of dermonecrosis compared to WT. Lair1 KO exhibited a pattern of increased inflammatory responses in infection and sterile immune stimulation, including increased production of proinflammatory cytokines and myeloid chemokines, neutrophil ROS, and collagen/ECM remodeling pathways. Notably, compared to WT, Lair1 KO infected skin had a similar bacterial burden and neutrophils and monocytes had equivalent S. aureus phagocytosis. These findings support a model in which lack of LAIR1 signaling results in an excessive inflammatory response that does not improve infection control. CTCL tissues harbored similar patterns of increased cytokine and collagen production, suggesting that high levels of LAIR2 in CTCL recapitulates Lair1 KO, causing inflammatory tissue damage and compromising host defense against S. aureus infection.

2024-07-31 | GSE269178 | 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