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PrrA modulates Mycobacterium tuberculosis response to nitric oxide

ABSTRACT: PrrA modulates Mycobacterium tuberculosis response to nitric oxide

PROVIDER: PRJNA817811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18363027.fastq.gz	Fastqsanger.gz
	SRR18363028.fastq.gz	Fastqsanger.gz
	SRR18363029.fastq.gz	Fastqsanger.gz
	SRR18363030.fastq.gz	Fastqsanger.gz
	SRR18363031.fastq.gz	Fastqsanger.gz

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PrrA modulates Mycobacterium tuberculosis response to nitric oxide

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

2022-06-23 | GSE198997 | GEO

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.

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

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

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Role of nitric oxide and nitric oxide synthase isoforms in pulmonary emphysema.

Project description:The purpose of this study is to comprehensively elucidate the role of nitric oxide and nitric oxide synthase isoforms in pulmonary emphysema using cap analysis of gene expression (CAGE) sequencing.

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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

Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide mediate signaling in plant defense.

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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

Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide mediate signaling in plant defense.

Project description:Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide- mediate signaling in plant defense. Nitric Oxide, Oleic acid, Salicylic acid, Arabidopsis, Defense Wild-type Col-0, mutant genotypes ssi2, ssi2 act1 and ssi2 sid2 with three biological replicates were analyzed (one array each)

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Nitric oxide modulates metabolic remodelling and immunometabolism in inflammatory murine macrophages

Project description:Classical stimulation of macrophages (MLPS/IFNγ) elicits the expression of inducible nitric oxide synthase (iNOS), generating large amounts of nitric oxide (NO) and inhibiting respiration. Consequent upregulation of glycolysis and a disrupted tricarboxylic acid (TCA) cycle underpin this switch to a pro-inflammatory phenotype. Here we show that the NOS cofactor tetrahydrobiopterin (BH4) modulates key aspects of metabolic remodelling in activated bone-marrow-derived macrophages (BMDMs) via NO production. Using two complementary mouse models that each lack the capacity for inducible NO generation, through different mechanisms, we reveal that NO regulates macrophage respiratory function via changes in the abundance of critical N-module subunits in Complex I, by HIF1α-mediated glycolytic remodelling, and by modulating levels of the critical TCA cycle metabolites, and inflammatory mediators, citrate, succinate, and itaconate. Taken together, our findings reveal new critical roles for iNOS-derived NO that are required for metabolic remodelling and cytokine production in macrophage inflammatory responses.

2019-05-31 | PXD010628 | Pride

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