Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-nucleus sequencing of liver cells from hepatocyte-specific Nampt knockout mice and WT littermates reveals major changes to the hepatocyte transcriptome in mice with necrosis

ABSTRACT: Single-nucleus sequencing of liver cells from hepatocyte-specific Nampt knockout mice and WT littermates reveals major changes to the hepatocyte transcriptome in mice with necrosis

PROVIDER: PRJNA728893 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14494832_1.fastq.gz	Fastqsanger.gz
	SRR14494832_2.fastq.gz	Fastqsanger.gz
	SRR14494833_1.fastq.gz	Fastqsanger.gz
	SRR14494833_2.fastq.gz	Fastqsanger.gz
	SRR14494834.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Role of hepatocyte NAMPT in fasting-induced liver gene expression

Project description:We tested they hypothesis that hepatocyte NAMPT mediates transcriptomic changes induced by fasting

2021-09-21 | GSE184395 | GEO

Role of NAMPT in liver gene expression in diabetic mice

Project description:We tested they hypothesis that hepatocyte NAMPT mediates transcriptomic changes in diabetic mice

2021-09-21 | GSE184513 | GEO

Hepatocyte-specific perturbation of the NAD+ biosynthetic pathways in mice promotes reversible NASH-like phenotypes

Project description:We report that the decreased expression of mitochondrial genes we observe in hepatocyte-specific Nampt knockout mice is normalized in primary hepatocytes, and that hepatocyte isolations causes major changes to the hepatocyte transcriptome for both knockouts and wildtype mice.

2021-11-03 | GSE173406 | GEO

Role of SIRT1 in NAMPT-induced liver gene expression

Project description:We tested they hypothesis that hepatocyte SIRT1 mediates transcriptomic changes induced by hepatocyte-specific NAMPT overexpression

2021-09-21 | GSE184394 | GEO

Hepatocyte-specific knockout of Nicotinamide phosphoribosyltransferase increases susceptibility for liver fibrosis in mice

Project description:We investigated the plasma and liver proteome changes in liver fibrosis in mice induced by hepatocyte-specific knockout of nicotinamide phosphoribosyltransferase (Nampt) upon a low-methionine, choline-free 60% high-fat (MCD) diet at multiple time points. We also investigated whether supplementation with nicotinamide riboside could alleviate liver injury and how the liver proteome changes upon NR supplementation.

2021-11-04 | PXD017170 | Pride

Liver tissue transcriptomic analysis of db/db mice expressing adenovirus-delivered GFP or NAMPT

Project description:Hypothesis is that NAMPT overexpression alters liver transcriptomics in genetically diabetic, obese db/db mice. We treated db/db mice n = 4 with adenovirus encoding GFP or NAMPT by tail-vein delivery.

2022-08-01 | E-MTAB-10984 | biostudies-arrayexpress

Hepatocyte-specific knockout of Nicotinamide phosphoribosyltransferase increases susceptibility for liver fibrosis in mice

Project description:Nicotinamide adenine dinucleotide (NAD+) supplementation has been suggested as a therapy against non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). We investigated whether hepatocyte-specific knockout of nicotinamide phosphoribosyltransferase (Nampt) caused increased susceptibility towards liver damage in mice fed a low-methionine, choline-free 60% high-fat (MCD) diet. Knockout mice (HNKO) accumulated less hepatic triglyceride than WT littermates after 3 weeks of MCD, but had increased scores for liver inflammation, necrosis, and fibrosis. We found that fibrosis, necrosis, and portal inflammation was also present in HNKO mice on a purified control diet (PD) but not in chow-fed HNKO mice due to a higher content of NAD+ precursors in the diet. The PD induced fibrosis within 3 days of exposure could be prevented by supplementation with the NAD+ precursor nicotinamide riboside (NR). When NR was supplied after fibrosis induction, hepatic NAD+ levels markedly increased, and portal inflammation was attenuated. The fibrosis phenotype was associated with a decreased abundance of proteins involved in oxidation and reduction processes, particularly for proteins in oxidative phosphorylation (OXPHOS). NR supplementation increased abundance of these proteins. High-resolution respirometry revealed that PD-fed HNKO mice had decreased oxygen consumption when stimulated with succinate, and a decrease in maximal uncoupled respiratory capacity. Conclusions: We show that HNKO mice have increased susceptibility towards liver fibrosis when dietary NAD+ content is restricted, and that low NAD+ levels can affect hepatic mitochondrial function. Furthermore, our data suggest NR treatment has potential for preventing liver damage and NASH progression.

2021-11-03 | GSE144443 | GEO

Role of hepatocyte NAMPT in fasting-induced liver gene expression

Project description:Role of hepatocyte NAMPT in fasting-induced liver gene expression

| PRJNA764442 | ENA

PR-SET7 inactivation causes hepatocyte necrosis and spontaneous development of hepatocellular carcinoma derived from ductal progenitor cells

Project description:PR-SET7-mediated histone-4 lysine-20 methylation has been implicated in mitotic condensation, DNA damage response and replication licencing. Here we show that PR-SET7 function in the liver is pivotal for maintaining genome integrity. Hepatocyte-specific deletion of PR-SET7 in mouse embryos resulted in G2 arrest followed by massive cell death and defect in liver organogenesis. Inactivation at postnatal stages caused cell duplication-dependent hepatocyte necrosis with unusual features of autophagy, termed "endonucleosis". Necrotic death was accompanied by inflammation, fibrosis and compensatory growth induction of neighboring hepatocytes and resident ductal progenitor cells. Prolonged necrotic-regenerative cycles coupled with oncogenic STAT3 activation replaced pre-existing hepatocytes with hepatocellular carcinoma derived entirely from ductal progenitor cells. Hepatocellular carcinoma in these mice displays a cancer stem cell gene signature specified by the co-expression of ductal progenitor markers and oncofetal genes. Mice carrying hepatocyte specific inactivation of PR-SET7 were generated in order to investigate the function of PR-SET7 histone methyl transferase in liver organogenesis, hepatocyte proliferation and liver regeneration. P15 WT mice were injected intra-peritoneally (ip) with 25ml per kg DEN (diethyl nitrosamine). Mice were examined for RNA expression at 8 months old.

2014-08-01 | E-GEOD-49555 | biostudies-arrayexpress

Analysis of liver RNA from SRSF3 hepatocyte knockout mice versus wild-type littermates

Project description:Livers from three SRSF3HKO mice and 3 wild-tyope littermates were used to analyze changes in exon utilization and gene expression.

2012-12-01 | GSE35686 | 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