Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PrrA modulates Mycobacterium tuberculosis response to nitric oxide

ABSTRACT: The purpose of this study was to understand the impact of prrA overexpression on global M. tuberculosis transcriptional response to nitric oxide.

ORGANISM(S): Mycobacterium tuberculosis

PROVIDER: GSE198997 | GEO | 2022/06/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

PrrA modulates Mycobacterium tuberculosis response to nitric oxide

Project description:PrrA modulates Mycobacterium tuberculosis response to nitric oxide

| PRJNA817811 | ENA

PrrA modulation of Mycobacterium tuberculosis response to nitric oxide is critically regulated by serine/threonine protein kinases

Project description:The purpose of this study was to understand how prevention of serine/threonine protein kinase (STPK) phosphorylation of PrrA impacts PrrA modulation of M. tuberculosis transcriptional response to nitric oxide.

2022-06-23 | GSE198999 | GEO

Time course RNA-seq of Mycobacterium tuberculosis exposed to nitric oxide.

Project description:Mycobacterium tuberculosis is an intracellular human pathogen with the ability to resist and adapt to many adverse conditions it encounters upon infection. Among these, overcoming the production of nitric oxide by macrophages could be key for M. tuberculosis success. We have challenged M. tuberculosis with a sub-lethal concentration of nitric oxide and followed the transcriptomic response through RNA-seq for 48 hours.

2017-08-29 | E-MTAB-5557 | biostudies-arrayexpress

Mycobacterium tuberculosis under nitric oxide stress

Project description:To study the entire transcriptional and translational M. tuberculosis response from initial survival to eventual escape from nitric oxide (NO) stress, we exposed exponentially growing M. tuberculosis to 1 mM diethylenetriamine/nitric oxide (DETA/NO) and followed the adaptive response over 48 hours. Samples were obtained from two independent experiments performed in triplicate and we sampled aliquots for transcriptome profiling by RNA sequencing at 20 min, 2 h and 24 h and for mass spectrometry-based shotgun proteomics at 20 min, 40 min, 1 h, 2 h, 4 h, 8 h, 12 h, 24 h and 48 h post NO exposure.

2017-08-17 | PXD006039 | Pride

PrrA modulation of Mycobacterium tuberculosis response to nitric oxide is critically regulated by serine/threonine protein kinases

Project description:PrrA modulation of Mycobacterium tuberculosis response to nitric oxide is critically regulated by serine/threonine protein kinases

| PRJNA817808 | ENA

Mycobacterium bovis transcriptional response to nitric oxide

Project description:We used microarray hybridization to analyze the expression pattern of M. bovis after exposure to nitric oxide. In M. tuberculosis, this treatment has been shown to induce a response similar to the hypoxic stress. Results showed the up-regulation of 51 genes belonging to the DosR regulon. The most remarkable difference with M. tuberculosis was the lack of expression of narX and narK2 in M. bovis, both genes related to survival during hypoxic stress. We further confirm this by qRT-PCR and also explore differential activity at promoter level.

2009-12-17 | GSE15164 | GEO

Mycobacterium bovis transcriptional response to nitric oxide

2010-05-17 | E-GEOD-15164 | biostudies-arrayexpress

Inhibition of Respiration by Nitric Oxide Induces a Mycobacterium tuberculosis Dormancy Program

Project description:An estimated two billion persons are latently infected with Mycobacterium tuberculosis. The host factors that initiate and maintain this latent state and the mechanisms by which M. tuberculosis survives within latent lesions are compelling but unanswered questions. One such host factor may be nitric oxide (NO), a product of activated macrophages that exhibits antimycobacterial properties. Evidence for the possible significance of NO comes from murine models of tuberculosis showing progressive infection in animals unable to produce the inducible isoform of NO synthase and in animals treated with a NO synthase inhibitor. Here, we show that O2 and low, nontoxic concentrations of NO competitively modulate the expression of a 48-gene regulon, which is expressed in vivo and prepares bacilli for survival during long periods of in vitro dormancy. NO was found to reversibly inhibit aerobic respiration and growth. A heme-containing enzyme, possibly the terminal oxidase in the respiratory pathway, likely senses and integrates NO and O2 levels and signals the regulon. These data lead to a model postulating that, within granulomas, inhibition of respiration by NO production and O2 limitation constrains M. tuberculosis replication rates in persons with latent tuberculosis.

2007-08-22 | GSE8839 | GEO

Inhibition of Respiration by Nitric Oxide Induces a Mycobacterium tuberculosis Dormancy Program

2007-08-21 | E-GEOD-8839 | biostudies-arrayexpress

PrrA modulates Mycobacterium tuberculosis response to acidic pH and high chloride levels

Project description:The purpose of this study was to identify genes that are differentially expressed upon prrA overexpression, to reveal the impact of PrrA on global transcription in acidic pH and/or high chloride conditions.

2022-06-23 | GSE198998 | 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