Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis in brown adipose tissue of mice lacking the mitochondrial protein optic atrophy 1 (OPA1) in thermogenic adipocytes

ABSTRACT: Transcriptome analysis in brown adipose tissue of mice lacking the mitochondrial protein optic atrophy 1 (OPA1) in thermogenic adipocytes

PROVIDER: PRJNA906118 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22432900_1.fastq.gz	Fastqsanger.gz
	SRR22432900_2.fastq.gz	Fastqsanger.gz
	SRR22432901_1.fastq.gz	Fastqsanger.gz
	SRR22432901_2.fastq.gz	Fastqsanger.gz
	SRR22432902_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Transcriptome analysis in brown adipose tissue of mice lacking the mitochondrial protein optic atrophy 1 (OPA1) in thermogenic adipocytes

Project description:mRNA expression profiles from interscapular brown adipose (iBAT) tissue of 7-week-old OPA1 BAT KO mice and their WT counterparts.

2023-10-10 | GSE218907 | GEO

Opa1

Project description:Drosophila melanogaster Opa1, Optic atrophy 1, is differentially expressed in 12 experiment(s);

| FBgn0261276 | ExpressionAtlas

Opa1

Project description:Drosophila melanogaster Opa1, Optic atrophy 1, is expressed in 4 baseline experiment(s);

| FBgn0261276 | ExpressionAtlas

The mitochondrial fusion protein OPA1 is dispensable in the live

Project description:Mitochondria are critical for metabolic homeostasis of the liver, and thus, mitochondrial dysfunction is a major cause of liver diseases. Optic atrophy 1 (OPA1) is a mitochondrial fusion protein that also plays a role in cristae shaping. Hence, the OPA1 gene disruption has been shown to cause mitochondrial dysfunction. However, the role of OPA1 in liver function is poorly understood. In this study, we deleted OPA1 in fully developed mouse liver and examined its effect.

2023-10-30 | PXD040556 | Pride

opa1

Project description:Xenopus tropicalis opa1, optic atrophy 1 (autosomal dominant) [Source:Xenbase;Acc:XB-GENE-989058], is expressed in 1 baseline experiment(s);

| ENSXETG00000016841 | ExpressionAtlas

Heart proteome in Cox10 depending on Opa1 processing

Project description:Mitochondrial fusion and fission accompany adaptive responses to stress and altered metabolic demands. Inner membrane fusion and cristae morphogenesis depends on Optic Atrophy 1 (Opa1), which is expressed in different isoforms and is cleaved from a membrane-bound, long to a soluble, short form. Here, we have analyzed the physiological role of Opa1 isoforms and Opa1 processing by generating mouse lines expressing only one cleavable Opa1 isoform or a non-cleavable variant thereof. Our results show that expression of a single cleavable or non-cleavable Opa1 isoform preserves embryonic development and the health of adult mice. Opa1 processing is dispensable under metabolic and thermal stress, but prolongs lifespan and protects against mitochondrial cardiomyopathy in OXPHOS-deficient Cox10-/- mice. Mechanistically, loss of Opa1 processing disturbs the balance between mitochondrial biogenesis and mitophagy, suppressing cardiac hypertrophic growth in Cox10-/- hearts. Our results highlight the critical regulatory role of Opa1 processing, mitochondrial dynamics and metabolism for cardiac hypertrophy.

2024-08-10 | PXD048804 | Pride

Single cell gene expression profile of WT and Opa1 knockout OT-I T cells

Project description:The goal of our study was to compare the gene expression of both naïve and activated T cells deficient in the mitochondrial protein Optic atrophy 1 (Opa1) using single cell RNA sequencing. A growing amount of evidence has begun to illustrate that the requirements driving effector- and memory-destined CD8 T cells during an infection are not shared with adjuvanted vaccine responses. Short-lived effector cells are characterized metabolically by a highly glycolytic state driving energy and biomass production whereas vaccine-elicited T cells can meet these requirements through mitochondrial metabolism. Here we show that the mitochondrial protein Optic atrophy 1 (Opa1) is critical for rapidly dividing CD8 T cells in vivo. This requirement, contrary to prior published data, is most pronounced in effector CD8 T cells. More specifically, Opa1 supports proper cell cycle initiation, progression, and supports the viability and survival of CD8 T cells during immune responses to both infections and vaccine challenges

2025-04-12 | GSE263898 | GEO

OPA1 mutations associated with dominant optic atrophy affect mitochondrial fusion and cell death in a domain-specific manner

Project description:Our study uncovered the role of OPA1 BSE domain in modulation of mitochondrial dynamics and cell death, and characterized the related signaling pathways, hereby providing the insight into the understanding of the domain-specific effect of OPA1 on mitochondrial morphology and function.

2025-02-24 | GSE289826 | GEO

OPA1 mutations associated with dominant optic atrophy affect mitochondrial fusion and cell death in a domain-specific manner

Project description:OPA1 mutations associated with dominant optic atrophy affect mitochondrial fusion and cell death in a domain-specific manner

| PRJNA1225147 | ENA

Discovering genetic causes of optic atrophy syndromes through whole exome sequencing

Project description:The genetic defects leading to optic atrophy range from mitochondrial DNA (mtDNA) point mutations in LeberÃ¢Â€Â™s hereditary optic neuropathy (LHON), to dominant and recessive mutations affecting a cluster of nuclear genes implicated in mitochondrial dynamics. We performed WES in patients with an optic atrophy spectrum disorder, including retinal macular dystrophy and kidney insufficiency leading to transplantation, associated with mitochondrial DNA (mtDNA) depletion without accumulation of multiple deletions, to identify the genetic causes of this syndrome.

| EGAS00001003850 | EGA

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