Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of Mitochondrial Biogenesis and Tumor Bioenergetics for Glioma

ABSTRACT: Inhibition of Mitochondrial Biogenesis and Tumor Bioenergetics for Glioma

PROVIDER: PRJNA697963 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13580968_1.fastq.gz	Fastqsanger.gz
	SRR13580968_2.fastq.gz	Fastqsanger.gz
	SRR13580969_1.fastq.gz	Fastqsanger.gz
	SRR13580969_2.fastq.gz	Fastqsanger.gz
	SRR13580970_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Inhibition of Mitochondrial Biogenesis and Tumor Bioenergetics for Glioma [A172 and U87MG]

Project description:Inhibition of Mitochondrial Biogenesis and Tumor Bioenergetics for Glioma [A172 and U87MG]

| PRJNA749802 | ENA

Inhibition of Mitochondrial Biogenesis and Tumor Bioenergetics for Glioma

Project description:The obejctive of this study is to To establish the therapeutic role of Gamitrinib for gliomas in vitro and in vivo and to elucidate the anti-tumor mechanism of Gamitrinib in glioma cells. And the ultimate goal of this proposal is to identify a novel Gamitrinib-based combination therapy for primary and recurrent gliomas.

2022-02-16 | GSE165819 | GEO

Inhibition of Mitochondrial Biogenesis and Tumor Bioenergetics for Glioma [A172 and U87MG]

2022-02-16 | GSE180872 | GEO

Chronic Caloric Restriction Preserves Mitochondrial Function in Senescence Without Increasing Mitochondrial Biogenesis

Project description:Caloric restriction (CR) without malnutrition appears to mitigate many detrimental effects of aging, in particular the age-related decline in skeletal muscle mitochondrial function. Although the mechanisms responsible for this protective effect remain unclear, CR is commonly believed to increase mitochondrial biogenesis; a concept that is now demanding closer scrutiny. Here we show that lifelong CR in mice prevents age-related loss of mitochondrial function, measured in isolated mitochondria and permeabilized muscle fibers. We find that these beneficial effects of CR occur without increasing mitochondrial abundance. Furthermore, whole-genome expression profiling and large-scale proteomic surveys revealed expression patterns inconsistent with increased mitochondrial biogenesis. These observations, combined with lower protein synthesis rates support an alternative hypothesis that CR preserves mitochondrial function not by increasing mitochondrial biogenesis, but rather by decreasing mitochondrial oxidant emission, increasing antioxidant scavenging, thereby minimizing oxidative damage to cellular components. Cross-sectional comparison of skeletal muscle from young (8mo), old (24mo) and old caloric restricted mice, obtained from the colony maintained on behalf of the National Institute on Aging.

2013-01-01 | E-GEOD-36285 | biostudies-arrayexpress

Cardiomyocyte-specific PCSK9 deficiency compromises mitochondrial bioenergetics and heart function

Project description:Cardiomyocyte-specific PCSK9 deficiency compromises mitochondrial bioenergetics and heart function

| PRJNA738856 | ENA

Chronic Caloric Restriction Preserves Mitochondrial Function in Senescence Without Increasing Mitochondrial Biogenesis

2013-01-01 | GSE36285 | GEO

Mitochondrial protein import stress augments alpha-synuclein aggregation and neurodegeneration independent of bioenergetics

Project description:Several genetic and environmental risk factors for Parkinson’s disease have been identified that converge on mitochondria as central elements in the disease process. However, the mechanisms by which mitochondrial dysfunction contributes to neurodegeneration remain incompletely understood. Non-bioenergetic pathways of the mitochondria are increasingly appreciated, but confounding bioenergetic defects are a major barrier to experimental validation. Here, we describe a novel bioenergetics-independent mechanism by which mild mitochondrial protein import stress augments neurodegeneration. We induced this mitochondrial protein import stress in an established mouse model of Parkinson’s disease expressing the A53T mutated form of human alpha-synuclein (SNCA). Mice with import stress in addition to the A53T mutation demonstrated increased size of SNCA aggregates, co-aggregation of mitochondrial preproteins with SNCA protein, worsened neurodegeneration and changes in gene expression, as determined by whole-transcriptome RNA-sequencing analysis of the forebrain (striatum), cerebellum, spinal cord, as well as heart and skeletal muscle.

2023-10-08 | GSE236975 | GEO

Anti-Warburg effect elicited by mitochondrial biogenesis drives differentiation of glioblastoma cells into astroglial cells

Project description:Glioblastoma (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed to be potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established the induced differentiation model of GBM by using cAMP activators, which specifically directed GBM into astroglia. Next, transcriptomic and proteomic analyses uncovered oxidative phosphorylation and mitochondrial biogenesis were involved in induced differentiation of GBM. Further investigation showed dbcAMP reversed Warburg effect evidenced by increase of oxygen consumption and reduction of lactate production. Stimulated mitochondrial biogenesis downstream of CREB/PGC1α pathway triggered metabolic shift and differentiation. Blocking mitochondrial biogenesis by mdivi1 or silencing PGC1α abrogated differentiation, reversely over-expression of PGC1α elicited differentiation. In GBM xenograft models and patient-derived GBM samples, cAMP activators also induced tumor growth inhibition and differentiation. This study shows mitochondrial biogenesis and metabolic switch to oxidative phosphorylation drive the differentiation process of tumor cells.

2017-11-10 | GSE89745 | GEO

Mitochondrial biogenesis induced by PGC-1alpha

Project description:Microarray time-course of mouse myotubes transduced with the transcriptional co-activator PGC-1alpha, which is known to induce mitochondrial biogenesis in muscle cells. Keywords: time course

2006-04-03 | GSE4330 | GEO

Atomic Vacancies of Molybdenum Disulfide Nanoparticles Stimulate Mitochondrial Biogenesis

Project description:Atomic vacancies rich MoS2 nanoflowers stimulate mitochondrial function by reducing cellualr ROS generation and upregulating the expression of genes required for mitochondrial biogenesis.

2024-06-27 | GSE235996 | 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