Endogenous S-nitrosothiols protect against myocardial injury - Test2 - elhamkhani - TriplyDB

Endogenous S-nitrosothiols protect against myocardial injury

Endogenous S-nitrosothiols protect against myocardial injury

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Regulation of cardiovascular cellular processes by S-nitrosylation S-nitrosylation in cardiovascular signaling Dissection of a hypoxia-induced, nitric oxide-mediated signaling cascade The identification of nitric oxide as endothelium-derived relaxing factor Nitric oxide synthases in heart failure NADPH oxidases in heart failure: poachers or gamekeepers?Redox balance dynamically regulates vascular growth and remodeling Characterization of potential S-nitrosylation sites in the myocardium The emerging immunological role of post-translational modifications by reactive nitrogen species in cancer microenvironment Ventilatory responses during and following exposure to a hypoxic challenge in conscious mice deficient or null in S-nitrosoglutathione reductase.Skeletal muscle-specific genetic determinants contribute to the differential strain-dependent effects of hindlimb ischemia in mice.Compartmentalized connexin 43 s-nitrosylation/denitrosylation regulates heterocellular communication in the vessel wall.Nitric oxide regulates mitochondrial fatty acid metabolism through reversible protein S-nitrosylation.Estradiol-17beta stimulates specific receptor and endogenous nitric oxide-dependent dynamic endothelial protein S-nitrosylation: analysis of endothelial nitrosyl-proteome.Adenosine A1 receptor activation increases myocardial protein S-nitrosothiols and elicits protection from ischemia-reperfusion injury in male and female hearts Analysis of nitroso-proteomes in normotensive and severe preeclamptic human placentas.Estrogen-responsive nitroso-proteome in uterine artery endothelial cells: role of endothelial nitric oxide synthase and estrogen receptor-β Endogenous NO upon estradiol-17β stimulation and NO donor differentially regulate mitochondrial S-nitrosylation in endothelial cells.A novel suppressive effect of alcohol dehydrogenase 5 in neuronal differentiation.Increased stability of S-nitrosothiol solutions via pH modulations.Impaired S-nitrosylation of the ryanodine receptor caused by xanthine oxidase activity contributes to calcium leak in heart failure What can we learn about cardioprotection from the cardiac mitochondrial proteome?Redox regulatory mechanism of transnitrosylation by thioredoxin.Glutaredoxin-1 overexpression enhances neovascularization and diminishes ventricular remodeling in chronic myocardial infarction.S-nitrosylation Inhibits protein kinase C-mediated contraction in mouse aorta.Simultaneous measurement of protein oxidation and S-nitrosylation during preconditioning and ischemia/reperfusion injury with resin-assisted capture Importance of NO and its related compounds in enteric nervous system regulation of gut homeostasis and disease susceptibility S-nitrosothiol signals in the enteric nervous system: lessons learnt from big brother.Lymphocyte development requires S-nitrosoglutathione reductase.Protein S-nitrosylation in health and disease: a current perspective.Targeted deletion of GSNOR in hepatocytes of mice causes nitrosative inactivation of O6-alkylguanine-DNA alkyltransferase and increased sensitivity to genotoxic diethylnitrosamine.Exercise protects against myocardial ischemia-reperfusion injury via stimulation of β(3)-adrenergic receptors and increased nitric oxide signaling: role of nitrite and nitrosothiols.Endothelial ephrin-B2 is essential for arterial vasodilation in mice.A new paramagnetic intermediate formed during the reaction of nitrite with deoxyhemoglobin.Regulation of DNA repair by S-nitrosylation.Thioredoxin 1-mediated post-translational modifications: reduction, transnitrosylation, denitrosylation, and related proteomics methodologies.Priming of hypoxia-inducible factor by neuronal nitric oxide synthase is essential for adaptive responses to severe anemia.S-nitrosoglutathione reductase-dependent PPARγ denitrosylation participates in MSC-derived adipogenesis and osteogenesis S-nitrosylation in the regulation of gene transcription Promoting endothelial function by S-nitrosoglutathione through the HIF-1α/VEGF pathway stimulates neurorepair and functional recovery following experimental stroke in rats.

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Endogenous S-nitrosothiols protect against myocardial injury

http://www.wikidata.org/entity/Q24658413

description

2009 nî lūn-bûn

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2009 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2009 թվականի ապրիլին հրատարակված գիտական հոդված

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2009年の論文

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2009年學術文章

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Endogenous S-nitrosothiols protect against myocardial injury

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Proceedings of the National Academy of Sciences of the United States of America

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Endogenous S-nitrosothiols protect against myocardial injury

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Brian Lima

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Dawn Bowles

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Diana L Diesen

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Emily Messina

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Gregory K W Lam

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Howard A Rockman

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Jeffrey Nienaber

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Jonathan S Stamler

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Joshua M Hare

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Liang Xie

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S-nitrosothiols signal hypoxia-mimetic vascular pathology

A metabolic enzyme for S-nitrosothiol conserved from bacteria to humans

Essential roles of S-nitrosothiols in vascular homeostasis and endotoxic shock

Regulation of beta-adrenergic receptor signaling by S-nitrosylation of G-protein-coupled receptor kinase 2

Isolation of putative progenitor endothelial cells for angiogenesis

Protein S-nitrosylation: a physiological signal for neuronal nitric oxide

S-nitrosylation signaling in cell biology.

Akt-mediated activation of HIF-1 in pulmonary vascular endothelial cells by S-nitrosoglutathione

Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction.

Ex vivo pretreatment of bone marrow mononuclear cells with endothelial NO synthase enhancer AVE9488 enhances their functional activity for cell therapy.

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