Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse muscle tissue

ABSTRACT: Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse muscle tissue

PROVIDER: PRJNA420415 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse muscle tissue

Project description:Analysis of muscle from C57BL/6 mice expressing V338Y mutant mitochondrial ribosomal protein.

2021-01-29 | GSE107520 | GEO

Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse brain tissue.

Project description:Analysis of brain from C57BL/6 mice expressing V338Y mutant mitochondrial ribosomal protein.

2021-03-24 | GSE121395 | GEO

Transcriptome analysis of V336Y mutant mitochondrial ribosomal protein in human HEK293 cell line

Project description:Analysis of HEK293 cells lines expressing V336Y mutant mitochondrial ribosomal protein.

2018-10-26 | GSE101503 | GEO

Transcriptome analysis of V336Y mutant and G313R mutant mitochondrial ribosomal protein in human HEK293 cell line

Project description:Analysis of HEK293 cells lines expressing V336Y mutant and G313R mutant mitochondrial ribosomal protein

2022-12-22 | GSE121394 | GEO

Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse brain tissue.

Project description:Transcriptome analysis of V338Y mutant mitochondrial ribosomal protein in mouse brain tissue.

| PRJNA497257 | ENA

Transcriptome analysis of V336Y mutant mitochondrial ribosomal protein in human HEK293 cell line

Project description:Transcriptome analysis of V336Y mutant mitochondrial ribosomal protein in human HEK293 cell line

| PRJNA394695 | ENA

KDM5-mediated transcriptional activation of ribosomal protein genes alters translation efficiency to regulate mitochondrial metabolism.

Project description:Genes encoding the KDM5 family of transcriptional regulators are disrupted in individuals with intellectual disability (ID). To understand the link between KDM5 and ID, we generated five Drosophila strains harboring missense alleles analogous to those observed in patients. These alleles showed effects on neuroanatomical development, cognition, and other behaviors, in addition to a transcriptional signature that included the downregulation of many ribosomal protein genes. A similar transcriptional profile was observed in KDM5C knockout human glutamatergic neurons derived from induced pluripotent stem cells (iPSCs), suggesting a conserved role for KDM5 proteins in regulating ribosomal protein genes. Loss of ribosomal protein gene expression resulted in changes to neuronal ribosome composition. Moreover, we find that the translation efficiency of mRNAs required for mitochondrial metabolism was particularly affected upon reduction KDM5 in Drosophila neurons. Altered mitochondrial activity was confirmed through metabolomic studies that revealed decreased citric acid cycle activity. KDM5 therefore plays a key role in maintaining mitochondrial function that, when altered, could contribute to cognitive and behavioral phenotypes.

2023-11-08 | GSE245380 | GEO

MicroRNA-382 silencing induces a mitonuclear protein imbalance and activates the mitochondrial unfolded protein response in muscle cells

Project description:Proper mitochondrial function plays a central role in cellular metabolism. Various diseases as well as aging are associated with diminished mitochondrial function. Previously, we identified 19 miRNAs putatively involved in the regulation of mitochondrial metabolism in skeletal muscle, a highly metabolically active tissue. In the present study, these 19 miRNAs were individually silenced in C2C12 myotubes using antisense oligonucleotides, followed by measurement of the expression of 27 genes known to play a major role in regulating mitochondrial metabolism. Based on the outcomes, we then focused on miR-382-5p and identified pathways affected by its silencing using microarrays, investigated protein expression and studied cellular respiration. Silencing of miRNA-382-5p significantly increased the expression of several genes involved in mitochondrial dynamics and -biogenesis. Microarray analysis of C2C12 myotubes silenced for miRNA-382-5p revealed a collective downregulation of mitochondrial ribosomal proteins and respiratory chain proteins. This effect was accompanied by an imbalance between mitochondrial proteins encoded by the nuclear and mitochondrial DNA (1.35-fold, p<0.01) and an induction of HSP60 protein (1.31-fold, p<0.05), indicating activation of the mitochondrial unfolded protein response (mtUPR). Furthermore, silencing of miR-382-5p reduced basal oxygen consumption rate by 14% (p<0.05) without affecting mitochondrial content, pointing towards a more efficient mitochondrial function as a result of improved mitochondrial quality control. Taken together, silencing of miR-382-5p induces a mitonuclear protein imbalance and activates the mtUPR in skeletal muscle, a phenomenon that was previously associated with improved longevity.

2018-08-28 | GSE116786 | GEO

KDM5-mediated transcriptional activation of ribosomal protein genes alters translation efficiency to regulate mitochondrial metabolism II.

2023-10-23 | GSE245515 | GEO

Ribosomal mistranslation leads to silencing of the unfolded protein response and increased mitochondrial biogenesis

Project description:Translation fidelity is the limiting factor in the accuracy of gene expression. With an estimated frequency of 10-4, errors in mRNA decoding occur in a mostly stochastic manner. Little is known about the response of higher eukaryotes to chronic loss of ribosomal accuracy as per an increase in the random error rate of mRNA decoding. Here, we present a global and comprehensive picture of the cellular changes in response to translational accuracy in mammalian ribosomes impaired by genetic manipulation. In addition to affecting established protein quality control pathways, such as elevated transcript levels for cytosolic chaperones, activation of the ubiquitin-proteasome system, and translational slowdown, ribosomal mistranslation led to unexpected responses. In particular, we observed increased mitochondrial biogenesis associated with import of misfolded proteins into the mitochondria and silencing of the unfolded protein response in the endoplasmic reticulum. This study describes the metabolomic analysis of HEK293 cells lines expressing mutant ribosomal protein RPS2 (human A226Y). RPS2 A226Y mutation has been shown to cause misreading and readthrough. Results provide insight into the response to chronic mistranslation in mammalian cells.

2019-09-17 | MTBLS106 | MetaboLights

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