Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The role of TEFM in mitochondrial gene expression

ABSTRACT: The role of TEFM in mitochondrial gene expression

PROVIDER: PRJNA397134 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5896070_1.fastq.gz	Fastqsanger.gz
	SRR5896070_2.fastq.gz	Fastqsanger.gz
	SRR5896071_1.fastq.gz	Fastqsanger.gz
	SRR5896071_2.fastq.gz	Fastqsanger.gz
	SRR5896072.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 23

Similar Datasets

Prostate Cancer mitochondrial DNA heteroplasmies and mitochondrial gene expression

Project description:Altered mitochondrial function in prostate cancer was characterized using paired malignant/non-malignant (benign) tissue samples. Mitochondrial DNA heteroplasmies (mtDNA-NGS) and mitochondria associated gene transcript levels (RNAseq-NGS) were analyzed and correlated to mitochondrial respiration (high-resolution respirometry), to each other and to the tumor stage and grade.

| EGAS00001004186 | EGA

The role of TEFM in mitochondrial gene expression [smallRNA]

Project description:We investigated the role of TEFM in vivo by creating heart- and skeletal-muscle specific knockout of this gene. We identified that TEFM is required for the processivity of POLRMT and its loss leads to significantly decreased mitochondrial transcription.

2019-04-01 | GSE102253 | GEO

Gene expression analaysis of the lateral spreading tumor

Project description:Primary outcome(s): Gene expression of targeted genes

| 2625389 | ecrin-mdr-crc

Mitochondrial gene expression is required for platelet function and blood clotting

Project description:Platelets are anucleate blood cells that contain mitochondria and regulate blood clotting in response to injury. Mitochondria contain their own gene expression machinery which relies on nuclear encoded factors for the biogenesis of the oxidative phosphorylation (OXPHOS) system to produce energy, ions and metabolites required for thrombosis. The autonomy of the mitochondrial gene expression machinery from the nucleus is not known and platelets provide a valuable model to understand the importance of mitochondrial gene expression in anucleate cells. We generated three different platelet-specific conditional knockout mouse models, each lacking a gene that is essential for mitochondrial gene expression at the level of RNA processing, stability and translation (Elac2Pf4?/Pf4?, Ptcd1Pf4?/Pf4 and Mtif3Pf4?/Pf4?). Loss of ELAC2, PTCD1 or MTIF3, leads to increased megakaryocyte ploidy, elevated circulating levels of reticulated platelets, thrombocytopenia and consequent extended bleeding time. Furthermore, impaired RNA metabolism also reduced agonist induced platelet activation. Transcriptomic and proteomic analyses showed that mitochondrial gene expression and protein synthesis facilitate fibrinolysis, haemostasis and blood coagulation in response to injury.

2023-11-01 | PXD045688 | Pride

The role of TEFM in mitochondrial gene expression [TruSeq]

2019-04-01 | GSE102254 | GEO

Ribonucleotide synthesis by NME6 fuels mitochondrial gene expression

Project description:Replication and expression of the mitochondrial genome depend on the sufficient supply ofnucleotide building blocks to mitochondria. Dysregulated nucleotide metabolism is detrimental tomitochondrial genomes and can destabilise mitochondrial DNA and trigger inflammation. Here, wereport that a mitochondrial nucleoside diphosphate kinase, NME6, supplies mitochondria withpyrimidine ribonucleotides to drive the transcription of mitochondrial genes. Perturbation of NME6leads to the depletion of mitochondrial transcripts, destabilisation of the electron transport chainand impaired oxidative phosphorylation. These deficiencies are rescued upon supplementation withpyrimidine ribonucleosides. Moreover, NME6 is required for the maintenance of mitochondrial DNAwhen the access to cytosolic pyrimidine deoxyribonucleotides is limited. Our results, therefore, shedlight on the importance of mitochondrial ribonucleotide salvage for the synthesis of RNA andmitochondrial gene expression.The repository contains two internal projects which are identified by the internal IDs: 0187 and 0196. The raw files are indicated by the internal ID, and each Supplementary Table contains a reference to the internal ID. The project with the ID 0187 contains whole cell (WC) and immunoprecipitation (IP) data. Please see the file: SampleNamesForProjects.xlsx for more details.

2023-05-04 | PXD038391 | Pride

MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

Project description:MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factor—Host Cell Factor (HCF)-1—contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYC–HCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYC–HCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYC–HCF-1 interaction as a focal point for development of novel anti-cancer therapies.

2020-07-15 | ST001429 | MetabolomicsWorkbench

Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2

Project description:Metabolic engagement is intrinsic to immune cell function. Prostaglandin E2 (PGE2) has been shown to modulate macrophage activation, yet how PGE2 might affect metabolism is unclear. Here we show that PGE2 causes mitochondrial membrane potential (Δψm) to dissipate in interleukin-4 activated macrophages (M(IL-4)). Effects on Δψm are a consequence of PGE2-initiated transcriptional regulation of genes in the malate-aspartate shuttle (MAS), particularly GOT1. Reduced Δψm causes alterations in the expression of 126 voltage regulated genes (VRGs) including Resistin like molecule-α (RELMα), a key marker of M(IL-4), and genes that regulate cell cycle, The transcription factor ETS variant 1 (ETV1) plays a role in the regulation of 38% of the VRGs. These results reveal ETV1 as a Δψm-sensitive transcription factor, and Δψm as a mediator of mitochondrial-directed nuclear gene expression.

2021-09-08 | PXD010997 | Pride

Identification of proteins differentially regulated upon perturbed mitochondrial gene expression

Project description:The aim of this project was to search for the new factors engaged in mitochondrial nucleic acids metabolism under stress conditions. To this end we treated human 293 cells with mitochondrial replication/transcription inhibitor ethidium bromide and we compared proteomes of untreated vs treated cells. We were looking for the proteins whose level would be differentially regulated in response to disturbed mitochondrial gene expression. In our studies we utilized a stable 293 cell line that inducible expresses a fusion of EGFP with mitochondria targeting sequence. This approach enabled us to control mitochondrial import by analysis of the abundance of mitochondrial EGFP marker. We isolated highly purified mitochondria from the cells, lysed them and subjected protein extracts to labelling with iTRAQ reagents. We performed quantitative analysis of stress- induced changes of human mitochondrial proteome with the use of MaxQuant software.

2019-06-13 | PXD012055 | Pride

Differential Protein and Gene Expression in Endocrine and Neuroendocrine Tumors (NET)

Project description:Interventions: Group 1: Quantitative Expression Analysis of the proteom and gene Expression of Primary Tumor, normal tissue, and metastases Primary outcome(s): Disease associated Proteins and Genes Study Design: Allocation: ; Masking: ; Control: ; Assignment: ; Study design purpose: basic science

| 2431957 | ecrin-mdr-crc

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