Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Excessive O-GlcNAcylation causes heart failure and sudden death

ABSTRACT: Excessive O-GlcNAcylation causes heart failure and sudden death

PROVIDER: PRJNA553816 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9668830_1.fastq.gz	Fastqsanger.gz
	SRR9668830_2.fastq.gz	Fastqsanger.gz
	SRR9668840_1.fastq.gz	Fastqsanger.gz
	SRR9668840_2.fastq.gz	Fastqsanger.gz
	SRR9668850_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Excessive O-GlcNAcylation causes heart failure and sudden death

Project description:Heart failure is a leading cause of death worldwide, and failing heart muscle is marked by increased O-GlcNAcylation (OGN). It is unknown if excessive OGN contributes to cardiomyopathy and heart failure. OGN modifies serines and threonines, total OGN levels follow cellular nutrient and metabolic flux in addition to net activity of O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). We developed new transgenic mouse models with myocardial delimited over-expression of OGA and OGT, and found that OGT transgenic mice developed severe cardiomyopathy and premature death. In contrast, OGA transgenic hearts had normal function, but were resistant to pathological stress. Interbreeding OGA transgenic mice rescued cardiomyopathy and premature death in OGT transgenic mice. RNA Seq and functional studies highlighted disrupted metabolism in hearts from OGT transgenic mice that was rescued by OGA transgenic interbreeding. Here we show excessive OGN causes cardiomyopathy, identify gene programs responsive to pathological OGN, and suggest attenuation of OGN may be an effective therapy for heart failure.

2021-07-10 | GSE134121 | GEO

Epilepsy related sudden death

Project description:These samples include exome sequences of samples from patients who suffered Sudden Unexplained Death in Epilepsy

| EGAS00001000352 | EGA

Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT-BioLINCC)

Project description:Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT-BioLINCC)

| PRJNA1115818 | ENA

Sudden Death in the Young Case Registry

Project description:Sudden Death in the Young Case Registry

| PRJNA942023 | ENA

Sudden Death in the Young Case Registry

Project description:Sudden Death in the Young Case Registry

| PRJNA942024 | ENA

Lipidomics in (SIDS) Sudden Infant Death Syndrome

Project description:Serum samples were collected postmortem from infants dying of Sudden Infant Death Syndrome.

2017-06-05 | ST000673 | MetabolomicsWorkbench

Loss of cardiomyocyte CYB5R3 impairs redox equilibrium and causes sudden cardiac death

Project description:Loss of cardiomyocyte CYB5R3 impairs redox equilibrium and causes sudden cardiac death

| PRJNA849237 | ENA

Metabolomics Workbench ST000673 - GNPS - Lipidomics in (SIDS) Sudden Infant Death Syndrome

Project description:Serum samples were collected postmortem from infants dying of Sudden Infant Death Syndrome.

2018-08-02 | MSV000082713 | GNPS

Loss of cardiomyocyte CYB5R3 impairs redox equilibrium and causes sudden cardiac death

Project description:Sudden cardiac death (SCD) in patients with heart failure (HF) is allied with an imbalance in reduction-oxidation (redox) signaling in cardiomyocytes; however, the basic pathways and mechanisms governing redox homeostasis in cardiomyocytes are not fully understood. Here, we show that cytochrome b5 reductase 3 (CYB5R3), an enzyme known to regulate redox signaling in erythrocytes and vascular cells, is essential for cardiomyocyte function. Using a conditional cardiomyocyte-specific CYB5R3 knockout mouse, we discovered that deletion of CYB5R3 in male adult cardiomyocytes, but not female, causes cardiac hypertrophy, bradycardia, and SCD. The increase in SCD in CYB5R3 KO mice is associated with calcium mishandling, ventricular fibrillation, and cardiomyocyte hypertrophy. Molecular studies reveal that CYB5R3 KO hearts display decreased ATP, increased oxidative stress, suppressed coenzyme Q levels, and hemoprotein dysregulation. Lastly, from a translational perspective, we reveal that the high-frequency missense genetic variant rs1800457, which translates into a CYB5R3 T117S partial loss-of-function protein, associates with decreased event-free survival (~20%) in African Americans with HF with reduced ejection fraction (HFrEF). Together, these studies reveal a crucial role for CYB5R3 in cardiomyocyte redox biology and identify a new genetic biomarker for individuals in the African American population that may potentially increase the risk of death from HFrEF.

2023-06-14 | GSE206121 | GEO

Proteomic Differences in Hippocampus and Cortex of Sudden Unexplained Death in Childhood

Project description:Sudden unexplained death in childhood (SUDC) is death of a child over one year of age that is unexplained after review of clinical history, circumstances of death, and complete autopsy with ancillary testing. Multiple etiologies may cause SUDC, with parallels to sudden unexpected death in epilepsy (SUDEP) in SUDC with a history of febrile seizures, suggesting possible abnormalities in hippocampus and cortex. To identify molecular signaling pathways underlying SUDC, we performed label-free quantitative mass spectrometry on microdissected frontal cortex, hippocampal dentate gyrus (DG), and cornu ammonis (CA1-3) in SUDC (n=19) and pediatric control cases (n=19) with an explained cause of death.

2021-12-23 | MSV000088611 | MassIVE

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