Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide changes in OGT-deficient mouse liver tissue

ABSTRACT: Genome-wide changes in OGT-deficient mouse liver tissue

PROVIDER: PRJNA557230 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9856220_1.fastq.gz	Fastqsanger.gz
	SRR9856220_2.fastq.gz	Fastqsanger.gz
	SRR9856221_1.fastq.gz	Fastqsanger.gz
	SRR9856221_2.fastq.gz	Fastqsanger.gz
	SRR9856222_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Genome-wide changes in OGT-deficient mouse liver tissue

Project description:Over a billion people suffer from chronic liver diseases worldwide, which often leads to fibrosis and then cirrhosis. Treatments for fibrosis remain experimental, in part because no unifying mechanism has been identified that initiates liver fibrosis. O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) plays a pro-survival role under stress in many tissues. Here we report that OGT protects against hepatocyte necroptosis and initiation of liver fibrosis. Decreased O-GlcNAc levels were seen in patients with alcoholic liver cirrhosis and in mice with ethanol-induced liver injury. Liver-specific O-GlcNAc transferase (OGT) knockout (OGT-LKO) mice progressed to liver fibrosis at 10 weeks of age. OGT-deficient hepatocytes underwent necroptosis. These findings identify OGT as a key suppressor of hepatocyte necroptosis and OGT-LKO mice may serve as an effective spontaneous genetic model of liver fibrosis.

2019-11-04 | GSE134993 | GEO

Genome-wide changes in OGT-depleted mouse adipose tissue

Project description:Appetite control is key to combat obesity in an over-nutritious environment. Whether and how over-nutrition induces hyperphagia and obesity through the adipose-to-brain axis is unclear. O-linked beta-D-N-acetylglucosamine (O-GlcNAc) transferase (OGT) couples nutrient cues to O-GlcNAcylation of intracellular proteins at serine/threonine residues. Here we show that adipocyte OGT is essential for high fat diet-induced hyperphagia, but is dispensable for baseline food intake. Adipocyte OGT stimulates hyperphagia by transcriptional activation of de novo lipid desaturation and accumulation of anandamide (AEA), an endogenous appetite-inducing cannabinoid (CB). Pharmacological manipulation of peripheral CB1 signaling regulates hyperphagia in an adipocyte OGT-dependent manner. These findings define adipocyte OGT as a fat sensor that regulates peripheral lipid signals, and uncover an unexpected adipose-to-brain axis that induces hyperphagia and obesity.

2018-09-12 | GSE111735 | GEO

Genome-wide changes in OGT-depleted mouse adipose tissue

Project description:Genome-wide changes in OGT-depleted mouse adipose tissue

| PRJNA437991 | ENA

Transcriptome analysis of OGT-sufficient and OGT-deficient regulatory T (Treg) cells

Project description:To gain comprehensive insight into the OGT-dependent transcriptional program in Treg cells, we performed RNA-sequencing of isolated YFP+ Treg cells from Foxp3YFP-Cre/wtOgtwt/fl and healthy Foxp3YFP-Cre/wtOgtfl/fl females to avoid secondary changes in gene expression caused by inflammation. We were able to identify 269 differentially expressed genes including 154 downregulated and 115 upregulated with p values less than 0.01, OGT-deficient Treg cells had impaired suppressive function and attenuated IL2/STAT5 signaling pathway.

2018-12-21 | GSE116758 | GEO

Transcriptome analysis of OGT-sufficient and OGT-deficient regulatory T (Treg) cells

Project description:Transcriptome analysis of OGT-sufficient and OGT-deficient regulatory T (Treg) cells

| PRJNA480070 | ENA

Pancreatic Epithelial Single Cell RNAseq in OGT-deficient cells

Project description:Pancreatic Epithelial Single Cell RNAseq in OGT-deficient cells

| PRJNA542702 | ENA

Liver proteome and phospho-proteome of OGT (O-GlcNAc transferase) and OGA(O-GlcNAcase) mouse liver knockouts

Project description:Proteome and phospho-proteome of OGT, OGA liver knockouts, and pharmacological inhibition of OGA identifies numerous proteins, phospho-proteins, were either inversely or equivalently changed.

2024-03-18 | MSV000094350 | MassIVE

Genome wide binding sites of BAP1, HCF1 and OGT

Project description:We report the genome wide binding sites of BAP1, HCF1 and OGT in bone marrow derived macrophages. De-ubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor–1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo. OGT and HCF-1 levels were decreased by Bap1 deletion, indicating a critical role for BAP1 in stabilizing these epigenetic regulators. Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex may suppress CMML. A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans. For BAP1, bone marrow derived macrophages were used differentiated from bone marrow cells of BAP1-3X Flag Tagged KI mice we generated. For OGT and HCF1, bone marrow derived macrophages were used from BAP1 WT mice.

2012-11-07 | E-GEOD-40723 | biostudies-arrayexpress

OGT, H2B S112GlcNAc, TET2 ChIP-seq results

Project description:TET2 directly interacts with OGT, which is important for the chromatin association of OGT in vivo. Although this specific interaction does not regulate the enzymatic activity of TET2, it facilitates OGT-dependent histone O-GlcNAcylation. Moreover, OGT associates with TET2 at transcription starting sites (TSS). Down-regulation of TET2 reduces the amount of H2B S112 GlcNAc marks in vivo, which are associated with gene transcription regulation. We found that OGT interacts with TET2 tightly. Using ChIP-seq with specific antibodies, we tested the co-localization of TET2 and OGT in genome level.

2012-12-11 | E-GEOD-41720 | biostudies-arrayexpress

Pancreatic Epithelial Single Cell RNAseq in OGT-deficient cells

Project description:Single Cell RNAseq was performed to identify cell types and upstream regulators in pancreatic epithelial cells with or without OGT.

2020-03-23 | GSE131134 | 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