Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [RNA-seq]

ABSTRACT: Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [RNA-seq]

PROVIDER: PRJNA635821 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11873965_1.fastq.gz	Fastqsanger.gz
	SRR11873965_2.fastq.gz	Fastqsanger.gz
	SRR11873966_1.fastq.gz	Fastqsanger.gz
	SRR11873966_2.fastq.gz	Fastqsanger.gz
	SRR11873967_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory

Project description:Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory

| PRJNA635818 | ENA

Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [ChIP-seq]

Project description:Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [ChIP-seq]

| PRJNA635822 | ENA

Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-26 | GSE151440 | GEO

Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [ChIP-seq]

Project description:We report chromatin profiling of H3K27ac in hippocampus neuronal cells

2021-01-27 | GSE151439 | GEO

Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [RNA-seq]

Project description:We report the high-throughput sequencing of RNA expression in cultured neurons and the brain. We report the high-throughput sequencing of mRNA expression in primary cultured Neurons.

2021-01-27 | GSE151438 | GEO

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

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

Acetylation reprograms MITF target selectivity and residence time

Project description:Acetylation reprograms MITF target selectivity and residence time

| PRJNA573049 | ENA

Expression data from Prkch-/-Apoe-/- mouse

Project description:To examine function of PKCh for atherosclerosis, we compared the gene expression profiles of control Apoe-/- and Prkch-/-Apoe-/- mice by microarray analysis. In peritoneal macrophages, higher expression of Arginase, type II gene were found in Prkch-/-Apoe-/- cells. Expression of genes involved in cholesterol biosynthesis were upregulated in Prkch-/-Apoe-/- liver.

2016-07-31 | GSE37841 | GEO

RNAseq of isolated astrocytes and microglia from APPPS1E4fl/fl mice following astroycte APOE removal

Project description:The e4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease and has been shown to increase amyloid pathology relative to the presence of the e2 and e3 alleles. In the brain, apoE is primarily produced by astrocytes and under pathological conditions also by microglia. The cell-type-specific role of apoE in amyloid pathology, especially after amyloid plaque deposition, has not been fully elucidated. We generated APPPS1-21/Aldh1l1-Cre/ERT2/apoE4flox/flox and APPPS1-21/apoE4flox/flox mice. At 3.8-months-of-age, during the phase of rapid plaque growth, we administered tamoxifen to reduce astrocytic APOE4 and assessed mice at 6-months-of-age. One day before tamoxifen treatment, mice were injected with methoxy-X04, a blood-brain-barrier permeant fluorescent marker that labeled the pre-existing fibrillar amyloid plaques. By using this strategy, we were able to characterize pre-existing plaques prior to the loss of astrocytic APOE4 and to also analyze newly-formed amyloid plaques after the loss of astrocytic APOE4. Interestingly, astrocytic APOE4 deletion strongly reduced pre-existing plaques. It also prevented new plaque formation and decreased glial reactivity. Importantly, the removal of astrocytic APOE4 resulted in enhanced microglial and astrocytic phagocytic ability, which may contribute to the reduction of the amyloid pathology.

2021-09-30 | GSE183050 | 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