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Homo sapiens

ABSTRACT: Nitric oxide responsive transcriptomic changes are cell type dependent

PROVIDER: PRJDB17217 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR519798_1.fastq.gz	Fastqsanger.gz
	DRR519798_2.fastq.gz	Fastqsanger.gz
	DRR519799_1.fastq.gz	Fastqsanger.gz
	DRR519799_2.fastq.gz	Fastqsanger.gz
	DRR519800_1.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:Changes in DNA methylation by exposure to nitric oxide

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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)

2012-07-31 | E-GEOD-36797 | biostudies-arrayexpress

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

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Schistosoma mansoni

Project description:Nitric oxide-dependent changes in Schistosoma mansoni gene expression

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T cell cancer therapy requires CD40-CD40L activation of TNFα-iNOS-producing dendritic cells

Project description:The effectiveness of new cancer therapies such as checkpoint blockade and adoptive cell transfer of activated anti-tumor T cells requires overcoming immunosuppressive tumor microenvironments. We found that the activation of tumor-infiltrating myeloid cells to produce local nitric oxide is a prerequisite for adoptively transferred CD8+ cytotoxic T cells to destroy tumors. These myeloid cells are phenotypically similar to ‘Tip-DCs’ or nitric oxide- and TNFα-producing dendritic cells. The nitric oxide-dependent killing was tempered by coincident arginase 1 expression, which competes with iNOS for arginine, the substrate for nitric oxide production. Depletion of immunosuppressive CSF-1R-dependent arginase 1+ myeloid cells enhanced nitric oxide-dependent tumor killing. Tumor killing via iNOS was independent of the microbiota but dependent on the CD40-CD40L pathway and, in part, lymphotoxin alpha. We extended our findings in mice to uncover a strong correlation between iNOS, CD40 and TNF expression and survival in colorectal cancer patients. Our results identify a network of anti-tumor targets to boost the efficacy of cancer immunotherapies.

2016-09-14 | GSE74427 | GEO

Project description:Nitric oxide-dependent anaerobic ammonium oxidation

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Homo sapiens

Project description:Nitric oxide induces p53-mediated cell death in human nasal epithelial cells

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Dynamic nitrosation - palmitoylation of CD36 regulates serum lipids

Project description:Regulation of endothelial cell (EC) lipid content is crucial for cell and organ function. During obesity, ECs become lipid laden leading to lipotoxicity and endothelial dysfunction which further contribute to metabolic syndrome progression. Here, we demonstrate a novel pathway by which the endothelium, via eNOS-dependent nitrosation, inhibits excess lipid accumulation during hyperlipidemic conditions in obesity. In the vasculature, nitric oxide has been reported as a potent vasodilator. However, we highlight a new role for nitric oxide as a modulator of serum lipids. We show this occurs as a result of the downregulation of Cav1, a potent negative regulator of endothelial nitric oxide synthase, increasing EC endogenous nitric oxide synthesis. Using EC-specific Cav1 knockout mice, we are able to increase nitric oxide in vivo. This increased nitric oxide leads to nitrosation of cysteines 3 and 466 on the cytoplasmic tails of CD36, a fatty acid translocase, disrupting palmitoylation of these residues and subsequently inhibiting trafficking of CD36 to the plasma membrane. Together, this work suggests that CD36 nitrosation occurs as a protective mechanism to prevent lipotoxicity and EC dysfunction during the progression of metabolic syndrome.

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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

NO-deficient vs wild type Col-0 Arabidopsis seedlings

Project description:Nitric oxide regulates plant development and responses to stress. However, the mechanisms underlying its regulatory role are still poorly known, and the impact of endogenous NO on the genome-wide transcriptome of plants has not been studied. For that purpose, we compared the transcriptomes of NO-deficient nia1nia2, noa1-2 and nia1nia2noa1-2 mutant versus wild type Arabidopsis thaliana plants. A core comprising 66 NO-responsive genes with similar expression in all NO-deficient genotypes was identified. Among them, 46 were down- and 20 up-regulated in NO-deficient plants, and thus positively and negatively regulated by endogenous NO, respectively. Accordingly with changes in its transcriptome, the NO-deficient nia1nia2noa1-2 mutant accumulated anthocyanins and indolic glucosinolates, displayed abnormal iron homeostasis in shoots and roots, and also showed altered root sensitivity to hormones such as ABA, ET, CYK and IAA. Together the presented data suggest NO functions essentially as a modulator of hormone action. Compared analysis of the transcriptomes of 15-day old seedlings from 3 different nitric oxide (NO)-deficient mutant genotypes versus wild type background Col-0 (3 independent biological replicates per genotype). NO-deficient mutant seedlings in Col-0 background were the double nia1nia2 mutant in nitrate reductases (NR/NIA) 1 and 2 (abbreviated as nia); the noa1-2 mutant allele in Nitric Oxide Associated 1 (AtNOA1) (abbreviated as noa); and, the triple nia1nia2noa1-2 (abreviated as nino).

2012-11-01 | E-GEOD-41958 | biostudies-arrayexpress

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