Similar Datasets
Project description:The goal of this study was to measure the effects of nitric oxide exposure (using DETA NONOate as a nitric oxide donor) on transcription in Caulobacter.
2010-06-21 | GSE21139 | GEO
Project description:The goal of this study was to measure the effects of nitric oxide exposure (using DETA NONOate as a nitric oxide donor) on transcription in Caulobacter. Untreated Caulobacter crescentus were grown to a density of 0.3 (at OD660) in PYE medium (pH 7) in rolled culture tubes. DETA-NONOate treated Caulobacter crescentus were grown to a density of 0.3 (at OD660), and then treated with 100 mM DETA NONOate for 30 minutes.
2010-06-20 | E-GEOD-21139 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in F. verticillioides M3125 when exposed to 1.5 mM DETA NONOate for 30 minutes. Assessed in reference to unexposed M3125. DETA NONOate is a nitric oxide (NO) donor with a half-life of approximately 56 hours at 27°C, pH 7.4, to liberate 2 moles of NO per mole of parent compound.
2017-11-01 | GSE56827 | GEO
Project description:The molecular mechanism underlying the role of hippocampal hilar interneuron degeneration in temporal lobe epilepsy (TLE) remains unclear. Especially, very few studies have focused on the role of neuronal nitric oxide synthase (nNOS, encoded by Nos1) containing hilar interneurons in TLE. In the present study, Nos1 conditional knockout mice were constructed, and we found that selective deletion of Nos1 in hilar interneurons rather than dentate granular cells (DGCs) triggered epileptogenesis. The level of nNOS was downregulated in patients and mice with TLE. Nos1 deletion led to excessive epilepsy-like excitatory input circuit formation and hyperexcitation of DGCs. Replenishment of hilar nNOS protein blocked epileptogenic development and memory impairment in pilocarpine-induced TLE mice. Moreover, chronic treatment with DETA/NONOate, a slowly released exogenous nitric oxide (NO) donor, prevented aberrant neural circuits of DGCs and the consequent epileptogenesis without acute antiseizure effects. Therefore, we concluded that NO donor therapy may be a novel anti-epileptogenesis strategy, different from existing antiseizure medications (ASMs), for curing TLE.
2024-10-21 | GSE274303 | GEO
Project description:To analyze gene expression pattern in response to nitric oxde in Saccharomyces cerevisiae, we performed microarray analysis using yeast cells treated with a nitric oxide donor S-nitroso-N-acetyl-DL-penicillamine (SNAP). S. cerevisiae S288c strain was cultured in synthetic dextrose (SD) minimal medium up to log phase (OD600 = 1), and then treated with 100 micro molar of SNAP for 10, 30, or 60 min. After treatment with SNAP, cells were disrupted adn total RNA was extracted. We commissioned following experiments to BIO MATRIX RESEARCH Inc. Nitric oxide-induced gene expression in S. cerevisiae was measured at 10, 30, or 60 minutes after exposure to 100 micro molar of nitric oxide donor SNAP.
2014-09-30 | E-GEOD-61836 | biostudies-arrayexpress
Project description:Reactive nitrogen species (RNS) derived from dietary and salivary inorganic nitrates (NO3-) foment innate host defenses associated with the acidity of the stomach. The mechanisms by which these reactive species exert antibiotic activity in the gastric lumen are, however, poorly understood. To identify targets of RNS, the genetically tractable acid tolerance response (ATR) that enables enteropathogens to survive the harsh acidity of the stomach was screened for signaling pathways responsive to RNS. The nitric oxide (NO) donor spermine NONOate derepressed the Fur regulon that controls secondary lines of resistance against organic acids. Despite inducing a Fur-mediated adaptive response, acidified RNS largely boosted gastric host defenses as demonstrated by the fact that Salmonella bacteria exposed to spermine NONOate during mildly acidic conditions were not only shed in low amounts in feces, but also exhibited ameliorated oral virulence. NO prevented Salmonella from mounting a de novo ATR, but was unable to suppress an already functional protective response, indicating that RNS target regulatory cascades but not the effectors that defend against the rigors of gastric acidity. Transcriptional and translational analyses revealed that the PhoPQ signaling cascade is a critical ATR target of NO in rapidly growing Salmonella. Inhibition of PhoPQ signaling appears to contribute to most of the NO-mediated abrogation of the ATR in log phase bacteria, because the augmented acid sensitivity of phoQ-deficient Salmonella was not further enhanced after RNS treatment. Since PhoPQ-regulated acid resistance is widespread in enteric pathogens, the RNS-mediated inhibition of the Salmonella ATR described herein may represent a common component of the innate host defenses of the gastric lumen. Keywords: acid tolerance response, nitric oxide Microarray analyses were conducted comparing transcript levels of log-phase Salmonella cultured in minimal E salts + 0.4% glucose, pH 4.4 in the presence or absence of 250 µM spermine NONOate for 1 hour. Microarrays were performed in triplicate under identical conditions (3 biological replicates).
2010-05-26 | E-GEOD-9398 | biostudies-arrayexpress
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.
2021-01-18 | GSE164521 | GEO
Project description:Reactive nitrogen species (RNS) derived from dietary and salivary inorganic nitrates (NO3-) foment innate host defenses associated with the acidity of the stomach. The mechanisms by which these reactive species exert antibiotic activity in the gastric lumen are, however, poorly understood. To identify targets of RNS, the genetically tractable acid tolerance response (ATR) that enables enteropathogens to survive the harsh acidity of the stomach was screened for signaling pathways responsive to RNS. The nitric oxide (NO) donor spermine NONOate derepressed the Fur regulon that controls secondary lines of resistance against organic acids. Despite inducing a Fur-mediated adaptive response, acidified RNS largely boosted gastric host defenses as demonstrated by the fact that Salmonella bacteria exposed to spermine NONOate during mildly acidic conditions were not only shed in low amounts in feces, but also exhibited ameliorated oral virulence. NO prevented Salmonella from mounting a de novo ATR, but was unable to suppress an already functional protective response, indicating that RNS target regulatory cascades but not the effectors that defend against the rigors of gastric acidity. Transcriptional and translational analyses revealed that the PhoPQ signaling cascade is a critical ATR target of NO in rapidly growing Salmonella. Inhibition of PhoPQ signaling appears to contribute to most of the NO-mediated abrogation of the ATR in log phase bacteria, because the augmented acid sensitivity of phoQ-deficient Salmonella was not further enhanced after RNS treatment. Since PhoPQ-regulated acid resistance is widespread in enteric pathogens, the RNS-mediated inhibition of the Salmonella ATR described herein may represent a common component of the innate host defenses of the gastric lumen. Keywords: acid tolerance response, nitric oxide
2008-03-01 | GSE9398 | GEO
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
2012-08-01 | GSE36797 | GEO
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