Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of ANGPTL3 mAb on liver transcriptomes in LDLR-deficient mice

ABSTRACT: The effect of ANGPTL3 mAb on liver transcriptomes in LDLR-deficient mice

PROVIDER: PRJNA601449 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10899227.fastq.gz	Fastqsanger.gz
	SRR10899228.fastq.gz	Fastqsanger.gz
	SRR10899229.fastq.gz	Fastqsanger.gz
	SRR10899230.fastq.gz	Fastqsanger.gz
	SRR10899231.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

The effect of ANGPTL3 mAb on liver transcriptomes in LDLR-deficient mice

Project description:Purpose: The goal of this study was to evaluate the effect of ANGPTL3 inhibition on liver transcriptomes in LDLR KO mice. Methods: Mice were treated once weekly for 3 weeks with 25mg/kg control mAb or ANGPTL3 mAb. Livers were harvested 6 days after the last mAb treatment. Results: ANGPTL3 inhibition had no major impact on hepatic gene expression.

2020-07-05 | GSE143726 | GEO

Transcriptomic profile of ANGPTL3-deficient HepG2 cells

Project description:Transcriptomic profile of ANGPTL3-deficient HepG2 cells

| PRJNA970702 | ENA

Transcriptomic profile of ANGPTL3-deficient HepG2 cells

Project description:Cardiovascular disease is a leading cause of death worldwide, and inhibition of the hepatically secreted protein ANGPTL3 has emerged as an effective treatment for lowering low-density lipoprotein cholesterol (LDL), the cardinal risk factor for coronary artery disease (CAD). In this study, we examine the effects of complete genetic deficiency of ANGPTL3 on the hepatocyte transcriptome using a HepG2 cell culture model with the ANGPTL3 locus "knocked out" (KO) via CRISPR-Cas9.

2023-05-15 | GSE232045 | GEO

ANGPTL3 deficiency alters the lipid profile and metabolism of cultured hepatocytes and human lipoproteins

Project description:Even though the functions of ANGPTL3 in the circulation are relatively well characterized, many mechanistic questions regarding the molecular consequences of ANGPTL3 loss-of-function and protection against cardiovascular disease remain unanswered. To help understant the molecular mechanisms exerted by ANGPTL3 deficiency, we studied the alterations of ANGPTL3 loss-of-function in hepatocytes and plasma lipid molecular species profiles.

2023-04-06 | GSE229133 | GEO

Liver gene expression profiles of Tribbles-homolog1 (Trib1)/Ldl-receptor (Ldlr) double-knockout mice against Ldlr-knockout mice

Project description:Genetic variants at the TRIB1 (Tribbles-homolog 1) gene locus are strongly associated with plasma lipid traits and the risk of coronary artery disease in humans. In this study, we analyzed the consequences of Trib1-deficiency (Trib1-/-) on hepatic gene expression in mice on the atherosclerosis-susceptible LDL-receptor deficient (Ldlr-/-) background. Therefore, Trib1-/- mice were crossed onto the Ldlr-/- background to generate double knockout mice (Trib1-/-Ldlr-/-) and fed a semisynthetic, modified AIN76 diet (0.02% cholesterol, 4.3% fat). At 20 weeks of age, Trib1-/-Ldlr-/- mice and Trib1+/+Ldlr-/- control mice were sacrificed and liver tissue was snap frozen in liquid nitrogen and stored at -80°C until further processing. Total RNA was isolated from liver tissue (n=8 mice per genotype) and subjected to microarray gene expression analysis.

2023-03-15 | E-MTAB-12669 | biostudies-arrayexpress

The role of LDLR in intestinal inflammation

Project description:Low-density lipoprotein (LDL) is a risk factor for atherosclerosis, obesity, and other metabolic diseases, but its role in colitis is unknown. Here, we investigated the role of LDL in colitis by using LDL receptor deficient mice (Ldlr-/-). Wild-type and Ldlr-/- mice were fed with 3% DSS for 5 days and colons tissues were collected at day 8 post DSS treatment. We observed that Ldlr-/- mice are less susceptible to colitis. To understand the role of LDLR in colitis pathogenesis, we isolated RNA from colons of WT and Ldlr-/- mice and perfoemed RNA-seq. Our data show that the expression of inflamamtory genes are reduced in Ldlr-/- colons compared to wild-type. These data suggest that LDL is a potent endogenous trigger for intestinal inflammation.

2024-11-01 | GSE277062 | GEO

PCSK9 deficiency results in a specific shedding of excess LDLR in female mice only: Role of hepatic cholesterol

Project description:PCSK9 promotes the lysosomal degradation of cell surface LDL receptor (LDLR). We analyzed how excess LDLR generated by PCSK9 deficiency is differently handled in male and female mice to possibly unveil the mechanism leading to the lower efficacy of PCSK9 mAb on LDL-cholesterol levels in women. Analysis of intact or ovariectomized PCSK9 knockout (KO) mice supplemented with placebo or 17β-estradiol (E2) demonstrated that female, but not male mice massively shed the soluble ectodomain of the LDLR in the plasma. Liver-specific PCSK9 KO or alirocumab-treated WT mice exhibit the same pattern. This shedding is distinct from the basal one and is inhibited by ZLDI-8, a metalloprotease inhibitor pointing at ADAM10/ADAM17. In PCSK9 KO female mice, ZLDI- 8 raises by 80 % the LDLR liver content in a few hours. This specific shedding is likely cholesterol-dependent: it is prevented in PCSK9 KO male mice that exhibit low intra-hepatic cholesterol levels without activating SREBP-2, and enhanced by mevalonate or high cholesterol feeding, or by E2 known to stimulate cholesterol synthesis via the estrogen receptor-α. Liver transcriptomics demonstrates that critically low liver cholesterol in ovariectomized female or knockout male mice also hampers the cholesterol-dependent G2/M transition of the cell cycle. Finally, higher levels of shed LDLR were measured in the plasma of women treated with PCSK9 mAb. PCSK9 knockout female mice hormonally sustain cholesterol synthesis and shed excess LDLR, seemingly like women. In contrast, male mice rely on high surface LDLR to replenish their stocks, despite 80 % lower circulating LDL.

2022-09-22 | GSE205008 | GEO

Retinal transcriptomes of Plk3-deficient animals

Project description:Retinal transcriptomes of Plk3-deficient animals

| PRJNA304025 | ENA

Single-nucleus RNA-seq of aortas from Ldlr-/- and Ldlr-/-Trem2-/- atherosclerotic mice

Project description:Single-nucleus RNA-seq of aortas was performed in Ldlr-/- and Ldlr-/-Trem2-/- mice fed a high fat diet for 10 weeks

2024-01-12 | GSE243086 | GEO

Bulk RNA-sequencing in Ldlr-/- or Ch25h-/-;Ldlr-/- peritoneal macrophages treated with LPS

Project description:Here we study the effect of LPS in the transcriptome of thioglycollate-elicited peritoneal macrophages isolated from Ldlr knock out and Ch25h;Ldlr double knock out mice

2022-07-01 | GSE189079 | 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