Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nuclear-mitochondrial genetic mismatch elicits an interferon-mediated cellular immune response

ABSTRACT: Nuclear-mitochondrial genetic mismatch elicits an interferon-mediated cellular immune response

PROVIDER: PRJNA450844 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7030520.fastq.gz	Fastqsanger.gz
	SRR7030530.fastq.gz	Fastqsanger.gz
	SRR7030521.fastq.gz	Fastqsanger.gz
	SRR7030531.fastq.gz	Fastqsanger.gz
	SRR7030522.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 21

Similar Datasets

Nuclear-mitochondrial genetic mismatch elicits an interferon-mediated cellular immune response

Project description:In this study, we used mRNA-Seq and functional assays to investigate the transcriptomic and cellular responses to nuclear-mitochondrial genetic mismatches using the xenomitochondrial cybrid panel. RNA-Seq revealed a remarkable reprogramming of nuclear gene expression in response to variation in the mitochondrial genome that involved adaptive changes in cellular metabolism and cell cycle regulation. Unexpectedly, we found that nuclear-mitochondrial mismatch elicits a strong interferon-mediated cellular response

2018-11-01 | GSE113340 | GEO

Mismatch between mtDNA and nuclear DNA determines metabolism and healthy aging

Project description:We postulate here that the two singular characteristics of the mitochondrial oxidative phosphorylation system—the integration of three potentially antagonistic functions in the same structure and the double genetic origin of the components that assemble together in these molecular machines—make the evolution of an optimal system impossible. As a consequence the system is intrinsically mismatched and has to be continuously monitored, Adjusted and regulated in order to achieve the necessary and variable performance. Systematic transcriptomic, Metabolomic and biochemical evaluation of animals with identical nuclear DNA but different mtDNA haplotype strongly support the existence of intrinsic mismatch and reveals profound lifelong metabolic consequences on reactive oxygen species generation, Insulin signaling, Tendency towards obesity, And healthy ageing parameters, Including telomere atresia

2016-07-13 | GSE56933 | GEO

Mismatch oligonucleotides in human

Project description:Tiled regions surrounding 5 human genes as 36mers, HBG2, TIMP3, SYN3, FLNA, FBX07. The first three of these genes, we tiled with various mismatch oligos in addition to 'perfect match' oligos. Keywords: Mismatch hybridization experiment Tiled perfect match and various designs of mismatch oligonucleotide for several human genes. Goal was to observe the influence of various MM types on hybridization behavior in human, and compare it to yeast (see related slide).

2010-05-05 | E-GEOD-13172 | biostudies-arrayexpress

Mismatch oligonucleotides in human

2009-02-18 | GSE13172 | GEO

Pericentromeric hypomethylation elicits an interferon response in an animal model of ICF syndrome

Project description:Pericentromeric hypomethylation elicits an interferon response in an animal model of ICF syndrome

| PRJNA478246 | ENA

Mismatch oligonucleotides in yeast

Project description:Tiled 10kb region centered around ACT1 gene (YFL039C, CHROMOSOME 6 @ coords 48760-59195), double-stranded, 36mers at 1bp spacing, with mismatches and deletions; also tiled 6 genes of interest (YBL092W, YGR155W, YOL040C, YOR312C, YMR242C, YLR229C), coding strand only, 36mers at 1bp spacing, with some mismatches and deletions Keywords: Mismatch hybridization experiment Tiled perfect match and various designs of mismatch oligonucleotide for several yeast genes. Goal was to observe the influence of various MM types on hybridization behavior in yeast and compare it to human (see related slide).

2010-05-05 | E-GEOD-13174 | biostudies-arrayexpress

interferon-induced global cellular SUMOylation Changes

Project description:This proteomics dataset was generated to study the changes in SUMO site abundances between control cells and Interferon-alpha treated cells using SILAC. Cells were first fractionated into the cytoplasmic and nuclear fractions. SUMOylated proteins were then purified from these extracts by Ni-NTA via the 6xHIS tag on the SUMO3 construct. The proteins were then digested with trypsin and the peptides desalted on HLB cartridges. The SUMOylated peptides, which harbor an NQTGG remnant after tryptic digestion, were enriched with our anti-NQTGG antibody. The resulting peptides were injected on the orbitrap fusion instrument. The .raw files were analyzed with maxqunt.

| MSV000081525 | MassIVE

Nuclear barrier induction as a new modality of cellular senescence

Project description:Blocking of nucleocytoplasmic trafficking is an essential feature of replicative senescence (RS). However, whether nuclear barrier per se causes cellular senescence still remains elusive. Here, we show that nuclear barrier induced by blocking nucleocytoplasmic trafficking, especially nuclear export, elicits RS-like changes in SA-β-gal activity, DNA damage, and expression of cell cycle regulators. Comparative transcriptome analysis revealed that nuclear barrier-induced senescence (NBIS) was most similar in gene expression changes to RS compared to senescence induced by stresses (oxidative stress, DNA damage and oncogene), implying that nuclear barrier induces RS-like physiological senescence-associated changes. Shared senescence-related processes between NBIS and RS included lysosomal degradation, nuclear transport, and translation, resulting in coordinated reduction in transmission of extrinsic signals to nucleus and intracellular protein supply from nucleus. Notably, these processes were conserved in yeast aging. Therefore, we propose NBIS as a novel modality of cellular senescence, representing the fundamental nature of physiological aging in eukaryotes.

2021-06-17 | GSE112530 | GEO

Transcriptomic evaluation of mismatch repair defects

Project description:Using numerous isogenic models of mismatch repair defects we sought to understand how these defects influence global transcription

2018-09-08 | GSE119667 | GEO

Human DNA Mismatch Repair pathway LC-MSMS

Project description:The mismatch repair (MMR) family is a highly conserved group of proteins that function in correcting base-base and insertion-deletion mismatches generated during DNA replication. To systematically investigate the mismatch repair pathway, we conducted a proteomic analysis and identified MMR-associated protein complexes using a tandem-affinity purification coupled with mass spectrometry (TAP-MS) method. In total, we identified 262 high-confidence candidate interaction proteins (HCIPs).

2016-02-08 | PXD003014 | Pride

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