Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674. - Wikidata - wikimedia - TriplyDB

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

http://www.wikidata.org/entity/Q34615204

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"Oxygen Sensing" by Na,K-ATPase: These Miraculous Thiols Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions-A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance Protein glutathionylation in cardiovascular diseases The effects of buthionine sulfoximine treatment on diaphragm contractility and SERCA pump function in adult and middle aged rats Regulation of signal transduction by reactive oxygen species in the cardiovascular system Effect of protein S-glutathionylation on Ca2+ homeostasis in cultured aortic endothelial cells.Cytosolic H2O2 mediates hypertrophy, apoptosis, and decreased SERCA activity in mice with chronic hemodynamic overload.Nitroxyl (HNO): A novel approach for the acute treatment of heart failure Primary carnitine deficiency and sudden death: in vivo evidence of myocardial lipid peroxidation and sulfonylation of sarcoendoplasmic reticulum calcium ATPase 2.Nitroxyl (HNO) stimulates soluble guanylyl cyclase to suppress cardiomyocyte hypertrophy and superoxide generation.Dual mechanisms of HNO generation by a nitroxyl prodrug of the diazeniumdiolate (NONOate) class.Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase C674 promotes ischemia- and hypoxia-induced angiogenesis via coordinated endothelial cell and macrophage function.Redox signaling in cardiac myocytes.Nitroxyl enhances myocyte Ca2+ transients by exclusively targeting SR Ca2+-cycling.Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function.Soluble guanylate cyclase is required for systemic vasodilation but not positive inotropy induced by nitroxyl in the mouse.A device for rapid and quantitative measurement of cardiac myocyte contractility Regulation of cell physiology and pathology by protein S-glutathionylation: lessons learned from the cardiovascular system.Redox regulation of SERCA2 is required for vascular endothelial growth factor-induced signaling and endothelial cell migration S-glutathionylation of the Na,K-ATPase catalytic α subunit is a determinant of the enzyme redox sensitivity S-glutathiolation impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.S-nitrosylation: specificity, occupancy, and interaction with other post-translational modifications.HNO enhances SERCA2a activity and cardiomyocyte function by promoting redox-dependent phospholamban oligomerization SERCA Cys674 sulphonylation and inhibition of L-type Ca2+ influx contribute to cardiac dysfunction in endotoxemic mice, independent of cGMP synthesis.The effects of nitroxyl (HNO) on H₂O₂ metabolism and possible mechanisms of HNO signaling.Hydrogen peroxide-mediated SERCA cysteine 674 oxidation contributes to impaired cardiac myocyte relaxation in senescent mouse heart The NO/ONOO-cycle as the central cause of heart failure.The emergence of nitroxyl (HNO) as a pharmacological agent.Redox signaling in cardiovascular health and disease.Mechanotransduction and Metabolism in Cardiomyocyte Microdomains.Decreased Soluble Guanylate Cyclase Contributes to Cardiac Dysfunction Induced by Chronic Doxorubicin Treatment in Mice.S-nitrosylation of TRIM72 at cysteine 144 is critical for protection against oxidation-induced protein degradation and cell death.S-glutathiolation in life and death decisions of the cell.Cardiac inotropes: current agents and future directions.Physiological regulation of cardiac contractility by endogenous reactive oxygen species.Redox control of cardiac excitability.Oxidative stress and sarcomeric proteins.Nitroxyl (HNO) for treatment of acute heart failure.Tri-modal regulation of cardiac muscle relaxation; intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.

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P2860

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

http://www.wikidata.org/entity/Q34615204

description

2009 nî lūn-bûn

@nan

2009 թուականի Մարտին հրատարակուած գիտական յօդուած

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2009 թվականի մարտին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

@zh-hk

2009年論文

@zh-mo

2009年論文

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2009年论文

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name

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@ast

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@en

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@nl

type

label

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@ast

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@en

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@nl

prefLabel

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@ast

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@en

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674.

@nl

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CIRCRESAHA.108.188441

P1433

Circulation Research

P1476

Nitroxyl activates SERCA in cardiac myocytes via glutathiolation of cysteine 674

@en

P2093

Alicia Evangelista

http://www.w3.org/2001/XMLSchema#string

Jingmei Zhang

http://www.w3.org/2001/XMLSchema#string

Mario P Trucillo

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Wilson S Colucci

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P2860

Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation.

Nitroxyl anion exerts redox-sensitive positive cardiac inotropy in vivo by calcitonin gene-related peptide signaling.

Nitroxyl improves cellular heart function by directly enhancing cardiac sarcoplasmic reticulum Ca2+ cycling.

A biochemical rationale for the discrete behavior of nitroxyl and nitric oxide in the cardiovascular system.

Thiol oxidation in signaling and response to stress: detection and quantification of physiological and pathophysiological thiol modifications.

The pharmacology of nitroxyl (HNO) and its therapeutic potential: not just the Janus face of NO

Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the beta-adrenergic pathway.

NO- activates soluble guanylate cyclase and Kv channels to vasodilate resistance arteries.

S-Glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide.

Inhibition of yeast glycolysis by nitroxyl (HNO): mechanism of HNO toxicity and implications to HNO biology.

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scholarly article

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10.1161/CIRCRESAHA.108.188441

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6

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104

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Richard A Cohen

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2009-03-05T00:00:00Z

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19265039

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3046805

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