Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from intestine samples of mice lacking intestinal Pcyt1a, which encodes an enzyme that regulates phosphatidylcholine synthesis.

ABSTRACT: Phosphatidylcholine is a membrane lipid. To determine its role in the intestine, we deleted the gene that produces this lipid specificallly in intestinal epithelial cells and conducted expression analysis. We used microarray analysis to determine changes in gene expression that occur in the absence of intestinal phosphatidylcholine synthesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE110474 | GEO | 2021/02/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from intestine samples of mice lacking intestinal Pcyt1a, which encodes an enzyme that reguates phosphatidylcholine synthesis.

Project description:Phosphatidylcholine is a membrane lipid. To determine its role in the intestine, we deleted the gene that produces this lipid specificallly in intestinal epithelial cells and conducted expression analysis. We used microarray analysis to determine changes in gene expression that occur in the absence of intestinal phosphatidylcholine synthesis.

2021-02-04 | GSE129776 | GEO

Expression data from intestine samples of mice lacking intestinal Pcyt1a, which encodes an enzyme that reguates phosphatidylcholine synthesis.

Project description:Expression data from intestine samples of mice lacking intestinal Pcyt1a, which encodes an enzyme that reguates phosphatidylcholine synthesis.

| PRJNA532759 | ENA

Expression data from intestine samples of mice lacking intestinal Pcyt1a, which encodes an enzyme that regulates phosphatidylcholine synthesis.

Project description:Expression data from intestine samples of mice lacking intestinal Pcyt1a, which encodes an enzyme that regulates phosphatidylcholine synthesis.

| PRJNA433833 | ENA

Inhibiting phosphatidylcholine remodeling in adipose tissue increases insulin sensitivity [scRNA-Seq]

Project description:Cell membrane phosphatidylcholine composition is regulated by lysophosphatidylcholine acyltransferase (LPCAT); changes in membrane phosphatidylcholine saturation are implicated in metabolic disorders. Here, we identified LPCAT3 as the major isoform of LPCAT in adipose tissues and created adipocyte-specific Lpcat3-knockout mice to study adipose tissue lipid metabolism. Transcriptome sequencing and plasma adipokine profiling were used to investigate how LPCAT3 regulates adipose tissue insulin signaling. LPCAT3 deficiency reduced polyunsaturated phosphatidylcholines in adipocyte plasma membranes, increasing insulin sensitivity. LPCAT3 deficiency influenced membrane lipid rafts, which activated insulin receptors and AKT in adipose tissue, and attenuated diet-induced insulin resistance. Conversely, higher LPCAT3 activity in adipose tissues from ob/ob, db/db, and high-fat diet-fed mice reduced insulin signaling. Adding polyunsaturated phosphatidylcholines to mature human or mouse adipocytes in vitro worsened insulin signaling. We suggest that targeting LPCAT3 in adipose tissues to manipulate membrane phospholipid saturation is a new strategy to treat insulin resistance.

2024-07-16 | GSE234884 | GEO

Inhibiting phosphatidylcholine remodeling in adipose tissue increases insulin sensitivity [RNA-Seq]

2024-07-16 | GSE235302 | GEO

Global consequences of phosphatidylcholine reduction in Bradyrhizobium japonicum

Project description:Analysis of a Bradyrhizobium japonicum pmtA mutant. PmtA catalyzes the first of three consecutive methylation reactions leading to phosphatidylcholine (PC) formation in B. japonicum. Disruption of the pmtA gene results in a significantly reduced PC content causing a defect in symbiosis with the soybean host. This study provides the first insight into global transcriptomic changes of a bacterial phosphatidylcholine biosynthesis mutant. Cells of the pmtA mutant and the wild type were grown to mid-exponential phase in full medium (PSY) under aerobic culture conditions. Keywords: genetic modification Comparative analyis of the B. japonicum pmtA mutant and the wild type grown under aerobic culture conditions.

2008-04-17 | E-GEOD-11187 | biostudies-arrayexpress

Reciprocal regulation of phosphatidylcholine synthesis and H3K36 methylation programs metabolic adaptation

Project description:Reciprocal regulation of phosphatidylcholine synthesis and H3K36 methylation programs metabolic adaptation

| PRJNA752757 | ENA

Phosphatidylcholine synthesis in the developing small intestine.

Project description:1. Phosphatidylcholine synthesis in the foetal, newborn and adult small intestine of rats was studied by determination of cytidine diphosphocholine-1,2-diacylglycerocholine phosphotransferase (cholinephosphotransferase) and acyl-CoA-1-acyl-sn-glycerol-3-phosphocholine acyltransferase (lysophosphatidylcholine acyltransferase) activities and the incorporation of [1-14C]oleic acid into phosphatidylcholine. 2. Cholinephosphotransferase activity was low in foetal jejunum and ileum, increased 3-4 fold in the ileum by 6 days of age and by 12 days in the jejunum. Jejunal activity remained constant throughout weaning; ileal activity gradually decreased to values 25% of that of the jejunum. 3. Lysophosphatidylcholine acyltransferase activity was high in foetal jejunum and ileum, decreased 70% immediately after birth in the jejunum and increased to adult values by 12 days of age. Ileal activity decreased by 20% after birth, but decreased more rapidly at weaning to 30% of the activity in jejunum. 4. Initial rates and steady-state incorporation of [1-14C]oleic acid into phosphatidylcholine by jejunal rings of 10 day-old rats exceeded that observed in jejunal rings from adult rats by 2-4-fold. 5. In the postnatal jejunum, neither cholinephosphotransferase and lysophosphatidylcholine acyltransferase activities nor oleic acid incorporation were stimulated by cortisone administration in vivo.

| S-EPMC1161589 | biostudies-other

Global consequences of phosphatidylcholine reduction in Bradyrhizobium japonicum

2008-04-17 | GSE11187 | GEO

Phosphatidylcholine editing is critical to lipid homeostasis in Arabidopsis trigalactosyldiacylglycerol1 mutants

Project description:Lipid remodeling is crucial for plant responses to abiotic stress and metabolic disturbances. A key aspect of this process involves the modification of phosphatidylcholine (PC) acyl chains by lysophosphatidylcholine: acyl-CoA acyltransferases (LPCATs). To understand their role in lipid homeostasis, we studied the trigalactosyldiacylglycerol1 (tgd1) mutant, which exhibits significant increases in fatty acid synthesis and flux through PC due to disrupted inter-organelle lipid trafficking. We discovered that the elevated fatty acid synthesis in tgd1 is due to the posttranslational activation of plastidic acetyl-coenzyme A carboxylase (ACCase). Global transcriptomic profiling revealed 62 significantly upregulated genes in tgd1, with 27 (44%) involved in RNA and DNA modifications, suggesting a role for posttranscriptional mechanisms in adapting to lipid trafficking disruptions. Additionally, transcript levels of LPCATs and several genes regulating ACCase were moderately increased in tgd1. Genetic analysis showed that knocking out LPCAT1 and LPCAT2 was lethal in the tgd1 background. Furthermore, plants homozygous for lpcat2 and heterozygous for lpcat1 in the tgd1 background displayed reduced levels of PC and TAG, along with altered fatty acid compositions. Our findings provide mechanistic insights into fatty acid synthesis regulation and highlight the critical role of LPCATs in maintaining cellular lipid homeostasis when fatty acid production exceeds the cellular demand for membrane lipid synthesis.

2024-09-16 | PXD054661 | Pride

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