Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The role of Cebpb in Alcohol-associated Liver Disease development and resolution

ABSTRACT: The role of Cebpb in Alcohol-associated Liver Disease development and resolution

PROVIDER: PRJNA1158711 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30599169_1.fastq.gz	Fastqsanger.gz
	SRR30599169_2.fastq.gz	Fastqsanger.gz
	SRR30599170_1.fastq.gz	Fastqsanger.gz
	SRR30599170_2.fastq.gz	Fastqsanger.gz
	SRR30599171_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

The role of Cebpb in Alcohol-associated Liver Disease development and resolution

Project description:Abstinence is an important therapeutic intervention for patients with alcohol-associated liver disease (ALD). However, fibrosis improvement after cessation is not uniform and some patients do not improve. We aimed to use scATAC-seq analysis in a mouse model of ALD to define the mechanism of poor ALD resolution. We analyzed differentially accessible regions in livers from control, ALD, or 4 weeks post alcohol cessation mice and identified transcription factors activated in ALD that remained activated after alcohol withdrawal. The top hit was C/EBPβ. We found that hepatocyte specific Cebpb knockout prevented ALD development, while knockout at the time of alcohol cessation promoted fibrosis resolution.

2024-09-12 | GSE276692 | GEO

Sex specific role of KDM5B demethylase in Alcohol-associated Liver Disease development and resolution

Project description:Alcohol-associated liver disease (ALD) is a major cause of alcohol related mortality. Recently we identified hepatic demethylases KDM5B and KDM5C as important sex-specific epigenetic regulators of alcohol response in the liver. In this study we aimed to study the molecular mechanisms of KDM5-dependent ALD development and resolution. We found that alcohol induces pathological changes in cell-cell communication in the liver that are in part mediated by epigenetic changes in hepatocytes mediated by histone demethylase KDM5B. Using cell type specific knockout mice, we found that KDM5B histone demethylase was a key regulator of alcohol-induced epigenetic changes in hepatocytes. Moreover, it regulated hepatocytes-non-parenchymal cell crosstalk that promoted inflammation and fibrosis development in ALD. This mechanism was specific to females. In males KDM5B deficiency was not sufficient to prevent fibrosis development. In contrast KDM5B demethylase loss promoted fibrosis resolution in both males and females. This mechanism involved changes in hepatocyte-macrophage crosstalk and LXRα activation, which we identified to be critical for the fibrosis resolution process. CONCLUSION: In summary, KDM5B demethylase is a regulator of cell-cell crosstalk involved in disease progression in females and in disease resolution in both sexes.

2023-10-07 | GSE244240 | GEO

Sex specific role of KDM5B demethylase in Alcohol-associated Liver Disease development and resolution

Project description:Sex specific role of KDM5B demethylase in Alcohol-associated Liver Disease development and resolution

| PRJNA1021978 | ENA

The Integrated "Multiomics" Landscape at Peak Injury and Resolution From Alcohol-Associated Liver Disease

Project description:To investigate the the liver transcriptome at peak injury and during early and late resolution from alcohol-induced liver injury in mice

2022-06-06 | GSE205484 | GEO

Sex specific role of KDM5 demethylases in Alcohol-associated Liver Disease

Project description:Alcohol-associated liver disease (ALD) is a major cause of alcohol related mortality. The specific mechanisms responsible for ALD development and progression are not fully understood, and there is limited therapy for any stage of ALD. Sex differences are often disregarded in in genetic and mechanistic studies. We aimed to take an unbiased approach to define sex specific pathways in livers exposed to alcohol. METHODS: Mice were fed LieberDeCarli alcohol liquid diet for 3 weeks. To identify the role of Kdm5b and Kdm5c we injected mice with AAV-shControl at 2x10^11 gc per mouse or AAV-shKdm5b and AAV-Kdm5c vectors at 10^11 gc per mouse. To assess the role of AhR we injected mice with AAV-shControl or AAV-shAhR vectors at 10^11 gc per mouse. RESULTS: We found several pathways affected by alcohol in sex specific way and identified KDM5 demethylases as contributors to that specificity.

2022-02-08 | GSE195889 | GEO

The Integrated "Multiomics" Landscape at Peak Injury and Resolution From Alcohol-Associated Liver Disease

Project description:The Integrated "Multiomics" Landscape at Peak Injury and Resolution From Alcohol-Associated Liver Disease

| PRJNA845940 | ENA

Depletion of Mitochondrial Methionine Adenosyltransferase α1 Triggers Mitochondrial Dysfunction in Alcohol-Associated Liver Disease

Project description:Mitochondrial MATα1 is selectively depleted in alcohol-associated liver disease through a mechanism that involves the isomerase PIN1 and the kinase CK2. Alcohol activates CK2, which phosphorylates MATα1 at Ser114 facilitating interaction with PIN1, thereby inhibiting its mitochondrial localization. Blocking PIN1-MATα1 interaction increased mitochondrial MATα1 levels and protected against alcohol-induced mitochondrial dysfunction.

2022-02-17 | PXD030383 | Pride

Expression profile of human breast cancer cells with CEBPB overexpression

Project description:CEBPB contributes to the migration of breast cancer cells. We used microarrays to detail the mechanism of CEBPB with downstream targets that drive breast cancer cell migration. CEBPB were overexpressed in MDA-MB231 cell for RNA extraction and hybridization on Agilent microarrays. We sought to obtain the mechanisms of CEBPB with downstream proteins that drive breast cancer cell migration.

2015-03-31 | E-GEOD-67425 | biostudies-arrayexpress

Sex specific role of KDM5 demethylases in Alcohol-associated Liver Disease

Project description:Sex specific role of KDM5 demethylases in Alcohol-associated Liver Disease

| PRJNA802555 | ENA

Blockade of lL17 signaling reverses alcohol-induced liver injury, and excessive alcohol drinking in mice.

Project description:Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.

2020-04-07 | GSE137228 | 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