Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

PROVIDER: PRJNA1023383 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26261669.fastq.gz	Fastqsanger.gz
	SRR26261670.fastq.gz	Fastqsanger.gz
	SRR26261671.fastq.gz	Fastqsanger.gz
	SRR26261672.fastq.gz	Fastqsanger.gz
	SRR26261673.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

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

| PRJNA1024948 | ENA

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

| PRJNA1023382 | ENA

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

| PRJNA1024654 | 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 DDP38003 treatment on HFHC diet-induced NASH in mice

| PRJNA1025103 | ENA

Effect of miR-33 supression in hepatocytes in NAFLD and NASH

Project description:We perform sc-RNAseq in NASH livers from WT and miR-33-AlbCRE conditional knock-out mice. Liver were isolated from mice after 6 months of feeding a choline deficient high fat diet to analyze the effect of miR-33 deficiency specifically in hepatocytes and the crosstalk between hepatocytes and other cell types in the liver.

2024-10-01 | GSE259277 | 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

Hepatic steatosis promotes atherosclerosis progression via extracellular vesicles mediated inhibition of cholesterol efflux in foam cells

Project description:To determine the functional miRNA mediated the inhibition role of exosomes (EVs) on the, cholesterol efflux, miRNA sequencing was conducted to compare the expression profile of miRNA content in EVs isolated from primary hepatocytes of chow diet-fed ApoE-/- mice (Chow-EVs) or HFHC-fed ApoE-/- mice (HFHC-EVs).

2023-10-18 | GSE232919 | GEO

Effects of NAFLD/NASH on hepatic gene expression.

Project description:To characterize gene expression changes in arachidonic acid metabolism pathway genes in the presense of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) mice administered were administered an atherogenic diet for a period of four weeks. Administration of the atherogenic diet resulted in significant enrichment of the arachidonic acid metabolism pathway by gene set enrichment analysis (GSEA). The core enrichment subset of genes was down-regulated in mice administered the atherogenic diet and the majority of the genes that were down-regulated were cytochrome P450s. A total of 4 wild-type mice were administered a standard diet (STD; control group) and 4 wild-type mice were administered a HFHC diet (HFHC).

2014-01-03 | E-GEOD-53381 | biostudies-arrayexpress

Chromatin architecture as a checkpoint for NASH-associated liver injury

Project description:Nonalcoholic steatohepatitis (NASH) is a progressive liver disease that is characterized by liver injury, inflammation and fibrosis. NASH pathogenesis is linked to reprogramming of chromatin landscape in the liver that predisposes hepatocytes to stress-induced tissue injury. However, the molecular nature of the putative checkpoint that maintains chromatin architecture and preserves hepatocyte health remains elusive. Here we show that heterogeneous nuclear ribonucleoprotein U (hnRNPU), a nuclear matrix protein that governs chromatin architecture and gene transcription, is a critical factor that couples chromatin disruption to NASH pathogenesis. RNA-seq and ChIP-seq studies revealed an extensive overlap between hnRNPU occupancy and altered gene expression during NASH. Hepatocyte-specific inactivation of hnRNPU disrupted liver chromatin accessibility, activated the molecular signature of NASH and sensitized mice to diet-induced NASH pathogenesis. Mechanistically, hnRNPU deficiency stimulated the expression of a truncated isoform of TrkB that promotes inflammatory signaling in hepatocytes and stress-induced cell death. These findings illustrate a novel mechanism through which disruptions of chromatin architecture drive the emergence of disease-specific signaling patterns that promote liver injury and exacerbate NASH pathogenesis.

2019-09-10 | GSE131336 | 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