Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GNPS - ApoE KO additional experiments with bile acids

ABSTRACT: GNPS - ApoE KO Additional Experiments with Novel Bile Acids analyzed on Q Exactive. Standards, samples, and samples + spike-in BA.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Pieter Dorrestein

PROVIDER: MSV000084630 | GNPS | Wed Nov 27 22:25:00 GMT 2019

REPOSITORIES: GNPS

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Aortic macrophages and endothelial cells of apoE KO mice aortas after plaque regression induced apoE adenoviral transfer

Project description:Aortic macrophages and endothelial cells of apoE KO mice were sorted and analyzed by microarray 2 weeks after regression was induced by adenoviral transfer of apoE. Aortic macrophages (CD45+ F4/80+ CD11b+) and endothelial cells (CD45- CD31+) were sorted from apoE KO mice and the RNA extracted and hybridized to Affymetrix Mouse Gene 1.0 ST array. We pooled aortas from 5 mice for each sort.

2015-01-01 | E-GEOD-42691 | biostudies-arrayexpress

Aortic macrophages and endothelial cells of apoE KO mice aortas after plaque regression induced apoE adenoviral transfer

Project description:Aortic macrophages and endothelial cells of apoE KO mice were sorted and analyzed by microarray 2 weeks after regression was induced by adenoviral transfer of apoE.

2015-01-01 | GSE42691 | GEO

GNPS - Mouse Feces APOE KO FXR KO IHC Haddad

Project description:Mouse fecal samples from APOE KO and APOE KO FXR KO animals under high fat and high cholesterol (HFHC) diet exposed to intermittent hypoxia and hypercapnia (IHC). Untargeted LC-MS/MS acquisition was performed on a Vanquish UHPLC system coupled to a Q-Exactive Hybrid Quadrupole-Orbitrap (Thermo Fisher Scientific, Bremen, Germany). Chromatographic separation was performed on a Kinetex 1.7 um 100 A pore size C18 reversed phase UHPLC column 50 x 2.1 mm (Phenomenex, Torrance, CA)

2025-08-19 | MSV000098881 | GNPS

Effect of dietary cholesterol on gene expression in the liver of apoE-KO mice

Project description:Apolipoprotein E-knock out (apoE-KO) mouse is known as a model animal for atherosclerosis accompanied by spontaneous hypercholesterolemia. When apoE-KO mice were fed a chow supplemented with 1.25% cholesterol (high-Chol diet), cholesterol and bile acids were highly increased in the liver within a week. However, the amount of triacylglycerol (TG) in very low-density lipoprotein (VLDL), but not in the liver, was reduced by 78%. The epididymal adipose tissue was almost diminished in the long term. Cholesterol metabolism is tightly regulated by both cholesterol and its metabolites in the mammalian liver, but the regulatory mechanism of TG synthesis remains to be elucidated. To evaluate the impact of high-Chol diet for 1 week on gene expression in the liver of apoE-KO mice, DNA microarray analysis was performed with comparison to apoE-KO mice fed a normal chow. We found that mRNA expression related to lipid metabolism was suppressed by the high-Chol diet in the liver of apoE-KO mice, which includes beta-oxidation and glycerol-3-phosphate (G3P) pathway for TG synthesis. In particular, the mRNA and protein expression of lipin-1 and lipin-2 was markedly decreased. PGC-1?, which up-regulates the transcription of lipin-1, was also suppressed. Lipin is reported to function as a coactivator of PGC-1? and is an inducible amplifier of PPAR?, indicating that the suppression of genes involved in beta-oxidation could be induced by suppression of the lipins. These data using apoE-KO mice indicate that cholesterol and its metabolites are involved in regulating TG metabolism through a suppression of lipin-1 and lipin-2 in the liver. This research provides evidence for the mechanism of lipin expression in the liver. Apo E-KO mice at 10 weeks of age were fed normal chow (control) or high-Chol diet containing 1.25% cholesterol for 1 week. Three independent experiments were performed at each diet.

2011-08-07 | E-GEOD-27457 | biostudies-arrayexpress

Proteomic analysis of apoE-KO mice liver exposed to inhaled silicon dioxide.

Project description:ApoE-KO mice were treated with silicon monoxide for 16 weeks. Protein abundance changes in relation to untreated control were measured in liver samples fractionated to cytosol and mitochondria by SWATH-MS.

2023-03-11 | PXD028547 | Pride

Effect of dietary cholesterol on gene expression in the liver of apoE-KO mice

Project description:Apolipoprotein E-knock out (apoE-KO) mouse is known as a model animal for atherosclerosis accompanied by spontaneous hypercholesterolemia. When apoE-KO mice were fed a chow supplemented with 1.25% cholesterol (high-Chol diet), cholesterol and bile acids were highly increased in the liver within a week. However, the amount of triacylglycerol (TG) in very low-density lipoprotein (VLDL), but not in the liver, was reduced by 78%. The epididymal adipose tissue was almost diminished in the long term. Cholesterol metabolism is tightly regulated by both cholesterol and its metabolites in the mammalian liver, but the regulatory mechanism of TG synthesis remains to be elucidated. To evaluate the impact of high-Chol diet for 1 week on gene expression in the liver of apoE-KO mice, DNA microarray analysis was performed with comparison to apoE-KO mice fed a normal chow. We found that mRNA expression related to lipid metabolism was suppressed by the high-Chol diet in the liver of apoE-KO mice, which includes beta-oxidation and glycerol-3-phosphate (G3P) pathway for TG synthesis. In particular, the mRNA and protein expression of lipin-1 and lipin-2 was markedly decreased. PGC-1α, which up-regulates the transcription of lipin-1, was also suppressed. Lipin is reported to function as a coactivator of PGC-1α and is an inducible amplifier of PPARα, indicating that the suppression of genes involved in beta-oxidation could be induced by suppression of the lipins. These data using apoE-KO mice indicate that cholesterol and its metabolites are involved in regulating TG metabolism through a suppression of lipin-1 and lipin-2 in the liver. This research provides evidence for the mechanism of lipin expression in the liver.

2011-08-08 | GSE27457 | GEO

Gene expression in aortic roots of Apoe KO mice with Nod1 stimulation

Project description:To explore the mechanisms underlying progression of atherosclerosis provoked by Nod1 ligand stimulation, we performed microarray gene expression profiling of aortic roots of 6- and 9-week-old Apoe KO mice with or without oral FK565 administration. A gene ontology analysis of the genes up-regulated in FK565-administrated group at both time points showed that a number of biological process terms were associated with immune response. Among chemokine/cytokine genes, we observed that only 3 genes such as Ccl5, Ccl8 and Cxcl16 elevated more than 2-fold in response to oral administration of FK565 at both time points. An eight chip study using total RNA recovered from aortic roots in Apoe KO mice with or without FK565 administration, at the age of 6 and 9 weeks. Two independent experiments were performed in each group. In FK565-administrated groups, mice were orally administrated FK565 (50 µg) twice a week for 1 or 4 weeks from 5 weeks of age.

2014-11-06 | E-GEOD-48947 | biostudies-arrayexpress

Proteomic analysis of liver cytosol and mitochondria of apoE-KO mice treated with TUG-891.

Project description:ApoE-KO mice were treated with FFAR4 agonist TUG-891 for 16 weeks. Protein abundance changes in relation to untreated control were measured in liver samples fractionated to cytosol and mitochondria by SWATH-MS.

2024-08-09 | PXD028535 | Pride

Transcriptomic analysis of ApoE-KO/APOL1 mouse choroid plexus

Project description:Transcriptomic analysis of ApoE-KO/APOL1 mouse choroid plexus

| PRJNA1061484 | ENA

LPS stimulation of APOE knock-out iPSC-derived microglia with different ApoE isoforms

Project description:APOE is the main genetic modifier for late onset Alzheimer’s disease (LOAD). While an APOE2/APOE3/APOE4 allelic series is well established for LOAD risk and neuropathology, molecular mechanisms underlying isoform-dependent risk and relevance of ApoE-associated lipids remain elusive. Here, we studied the effects of LPS stimulation on APOE KO iPSC-derived microglia treated with different ApoE isoforms (ApoE2/E3/E4) pre-complexed with BODIPY-cholesteryl ester (CE) and HDL -/+ recombinant LDLR extracellular domain.

2024-11-10 | GSE250249 | 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