Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA Sequencing of transmitochondrial cybrids

ABSTRACT: RNA Sequencing of transmitochondrial cybrids revealed a downregulation of oxidative phosphorylation and nicotinamide metabolism in cybrids with patient mitochondria

ORGANISM(S): Homo sapiens

PROVIDER: GSE215859 | GEO | 2022/10/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of transmitochondrial cybrids (triple negative breast cancer cells in SUM159 background)

Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids.

2016-04-14 | GSE72319 | GEO

Gene expression profiling of transmitochondrial cybrids (triple negative breast cancer cells in SUM159 background)

2016-04-14 | E-GEOD-72319 | biostudies-arrayexpress

Mitochondrial 12S hypermethylation in HeLa cells and A1555G cybrids

2012-09-18 | GSE33780 | GEO

Transcriptome profiling of cybrids cells with and without m.14487T>C mutation

Project description:Transcriptome profiling is a sensitive strategy to uncover the change of mitochondrial to nucleus signaling due to the minor alternation of mitochondrial OXPHOS function. Therefore, we hypothesized that even a minor alternation of OXPHOS function can also remold transcriptome profiles in m.14487T>C mutant cybrid when compared with control cybrids. Our data suggest that a comparable mitochondrial OXPHOS function between m.14487T and m.14487C cybrids is not because of compensatory boost of mitochondrial biogenesis in m.14487C cybrids.

2020-05-19 | GSE131739 | GEO

Arabidopsis thaliana Cybrids - RNA Sequencing

Project description:Reciprocal cybrids reveal how organellar genomes affect plant phenotypes

| PRJEB35324 | ENA

Mitochondrial 12S hypermethylation in HeLa cells and A1555G cybrids

Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls. four samples with 12S rRNA hypermethylation (two cell lines, with two biological replicates each) versus four samples with basal 12S rRNA methylation (two cell lines, with two biological replicates each)

2012-09-18 | E-GEOD-33780 | biostudies-arrayexpress

Arabidopsis thaliana Cybrids - Whole Genome Sequencing

Project description:Reciprocal cybrids reveal how organellar genomes affect plant phenotypes

| PRJEB29654 | ENA

Metabolic reprogramming from fatty acid oxidation to glycolysis in a patient mutation knock-in mouse model of Barth Syndrome. [human]

Project description:Mitochondria are central for cellular metabolism and energy supply. Barth Syndrome (BTHS) is a severe disorder due to dysfunction of the mitochondrial cardiolipin acyl transferase tafazzin. Altered cardiolipin remodeling affects mitochondrial inner membrane organization and function of membrane proteins such as transporters and the oxidative phosphorylation (OXPHOS) system. Here, we describe a mouse model that carries a G197V exchange in tafazzin, corresponding to BTHS patient. TAZG197V mice recapitulate disease-specific pathology including cardiac dysfunction and reduced oxidative phosphorylation. We show that mutant mitochondria display defective fatty acid driven oxidative phosphorylation due to reduced levels of carnitine palmitoyl transferases. A metabolic switch in ATP production from OXPHOS to glycolysis is apparent in mouse heart and patient iPS cell-derived cardiomyocytes. An increase in glycolytic ATP production inactivates AMPK causing altered metabolic signaling in TAZG197V. Treatment of mutant cells with AMPK activator reestablishes fatty acid driven OXPHOS and protects mice against cardiac failure.

2023-07-15 | GSE221663 | GEO

Metabolic reprogramming from fatty acid oxidation to glycolysis in a patient mutation knock-in mouse model of Barth Syndrome.[mouse]

2023-07-15 | GSE221662 | GEO

Crosstalk from Non-Cancerous Mitochondria Can Inbibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways

Project description:Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitochondria are inhibited in cybrids with non-cancerous mitochondria. These results suggest the critical oncogenic regulation by motochondrial-nuclear cross talk and highlights rectifying motochondiral functional properties as a promising target in cancer therapy.

2019-03-21 | GSE128610 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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