Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Effect of TAK1 gene silencing in hepatocytes on SIKE deletion-led activation of HFHC-induced NASH in mice

PROVIDER: PRJNA1024654 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26298661.fastq.gz	Fastqsanger.gz
	SRR26298662.fastq.gz	Fastqsanger.gz
	SRR26298663.fastq.gz	Fastqsanger.gz
	SRR26298664.fastq.gz	Fastqsanger.gz
	SRR26298665.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Project description:Effect of SIKE gene deficiency in hepatocytes on HFHC-induced NASH in mice

| PRJNA1023383 | ENA

Project description:Effect of SIKE gene overexpression in hepatocytes on HFHC diet-induced NASH in mice

| PRJNA1024948 | ENA

Project description:Effect of indobufen treatment on HFHC diet-induced MAPK activation and NASH in Sike KO mice

| PRJNA1024667 | ENA

Project description:Effect of SIKE gene deficiency on PO-induced NASH of hepatocytes

| PRJNA1023382 | ENA

Wolf_et_al

Project description:Metabolic activation of CD8+ and NKT-cells causes NASH and HCC through cross-talk with hepatocytes. Mice that devloped HCC or NASH were compared to work out genomic differences of the two diseases. In order to characterise the importance of CCR2 (activation of monocytes) in the development of NASH and HCC CCR2 double-mutant mice were compared to CCR2 wildtype mice.

2014-06-01 | E-MTAB-2469 | biostudies-arrayexpress

MCLR-elicited hepatic fibrosis and carcinogenic gene expression changes persist in rats with diet-induced nonalcoholic steatohepatitis through a 4-week recovery period

Project description:Nonalcoholic steatohepatitis (NASH) causes liver extracellular matrix (ECM) remodeling and is a risk factor for fibrosis and hepatocellular carcinoma (HCC). Microcystin-LR (MCLR) is a hepatotoxin produced by fresh-water cyanobacteria that causes a NASH-like phenotype, liver fibrosis, and is also a risk factor for HCC. The focus of the current study was to investigate and compare hepatic recovery after cessation of MCLR exposure in healthy versus NASH animals. Male Sprague-Dawley rats were fed either a control or a high fat/high cholesterol (HFHC) diet for eight weeks. Animals received either vehicle or 30 µg/kg MCLR (i.p: 2 weeks, alternate days). Animals were euthanized at one of three time points: at the completion of the MCLR exposure period and after 2 and 4 weeks of recovery. Histological staining suggested that after four weeks of recovery the MCLR-exposed HFHC group had less steatosis and more fibrosis compared to the vehicle-exposed HFHC group and MCLR-exposed control group. RNA-Seq analysis revealed dysregulation of ECM genes after MCLR exposure in both control and HFHC groups that persisted only in the HFHC groups during recovery. After 4 weeks of recovery, MCLR hepatotoxicity in pre-existing NASH persistently dysregulated genes related to cellular differentiation and HCC. These data demonstrate impaired hepatic recovery and persistent carcinogenic changes after MCLR toxicity in pre-existing NASH.

2021-11-06 | GSE188231 | GEO

Dietary cholesterol promotes fatty liver-associated liver cancer by inducing aberrant genomic expression and mutations

Project description:We investigated the effects of cholesterol on nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) in diethylnitrosamine-injected mice fed high-fat high-cholesterol (HFHC) diet versus high-fat (HF) alone. mRNA microarray analysis was applied for expressional aberrations.

2018-09-27 | E-MTAB-6002 | biostudies-arrayexpress

Changes of hepatic gene expression in C57BL/6N male mice fed high-fat high-calorie fructose (HFHC) diet for 8 weeks

Project description:In murine NAFL/NASH models, high-fat high-calorie fructose (HFHC) diet fed for 16 weeks induces hepatic steatosis, inflammatory cells infilatration and early stage fibrosis. In addition, HFHC diet 16 weeks but not 8 weeks is accompanied with weight gain and insulin resistance. The aim of this study is to determine the gene expression changes in mouse liver by HFHC diet for 8weeks.

2021-12-08 | GSE154426 | GEO

Project description:Effect of indobufen treatment on HFHC diet-induced MAPK activation and NASH in mice

| PRJNA1024665 | ENA

Discovery of lipotoxicity-sensitive transcription factors in non-alcoholic steatohepatitis

Project description:Non-alcoholic fatty liver disease is continuum of disorders among which non-alcoholic steatohepatitis (NASH) is particularly associated with a negative prognosis. Hepatocyte lipotoxicity is one of the main pathogenic factors of liver fibrosis and NASH. However, the molecular mechanisms regulating this process are poorly understood. Here, we integrated transcriptomic and chromatin accessibility analyses from human liver and mouse hepatocytes to identify lipotoxicity-sensitive transcription factors. We found that the transcription factors MAFK and TCF4 were activated in liver from NASH patients and by mouse hepatocyte lipotoxicity. Genetic deletion of these transcription factors protected hepatocytes against saturated fatty acid oversupply. Notably, MAFK- and TCF4-regulated gene expression linked to lipotoxicity closely correlated with transcriptional patters in fibrosis progression in NASH patients. Collectively, our findings uncovered novel molecular insights into lipotoxicityinduced NASH, revealing the relevance and therapeutic potential of MAFK and TCF4 in human disease.

2022-07-08 | PXD026717 | Pride

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