Deficient ryanodine receptor S-nitrosylation increases sarcoplasmic reticulum calcium leak and arrhythmogenesis in cardiomyocytes. - Wikidata - awgldk - TriplyDB

Deficient ryanodine receptor S-nitrosylation increases sarcoplasmic reticulum calcium leak and arrhythmogenesis in cardiomyocytes.

Deficient ryanodine receptor S-nitrosylation increases sarcoplasmic reticulum calcium leak and arrhythmogenesis in cardiomyocytes.

http://www.wikidata.org/entity/Q36300139

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NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy Leaky RyR2 trigger ventricular arrhythmias in Duchenne muscular dystrophy Regulation of cardiovascular cellular processes by S-nitrosylation S-nitrosylation in cardiovascular signaling Signaling by gasotransmitters Ca(2+) signaling in the myocardium by (redox) regulation of PKA/CaMKII Nitric oxide synthases in heart failure Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance S-nitrosothiols and the S-nitrosoproteome of the cardiovascular system Molecular mechanisms of neuronal nitric oxide synthase in cardiac function and pathophysiology Obligatory role of neuronal nitric oxide synthase in the heart's antioxidant adaptation with exercise Characterization of potential S-nitrosylation sites in the myocardium Protein S-nitrosylation and cardioprotection Nitric oxide regulates cardiac intracellular Na⁺ and Ca²⁺ by modulating Na/K ATPase via PKCε and phospholemman-dependent mechanism Displacement-encoded and manganese-enhanced cardiac MRI reveal that nNOS, not eNOS, plays a dominant role in modulating contraction and calcium influx in the mammalian heart.The Subcellular Localisation of Neuronal Nitric Oxide Synthase Determines the Downstream Effects of NO on Myocardial Function Nitric oxide signalling and neuronal nitric oxide synthase in the heart under stress.Mitochondrial ion channels/transporters as sensors and regulators of cellular redox signaling.Impaired S-nitrosylation of the ryanodine receptor caused by xanthine oxidase activity contributes to calcium leak in heart failure Dantrolene suppresses spontaneous Ca2+ release without altering excitation-contraction coupling in cardiomyocytes of aged mice.S-nitrosation of mitochondrial connexin 43 regulates mitochondrial function.Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor-Ca2+ release channel by NADPH oxidase 4 NADPH oxidase-2 inhibition restores contractility and intracellular calcium handling and reduces arrhythmogenicity in dystrophic cardiomyopathy.Diesterified nitrone rescues nitroso-redox levels and increases myocyte contraction via increased SR Ca(2+) handling Stabilization of the skeletal muscle ryanodine receptor ion channel-FKBP12 complex by the 1,4-benzothiazepine derivative S107 Simultaneous measurement of protein oxidation and S-nitrosylation during preconditioning and ischemia/reperfusion injury with resin-assisted capture Protein S-nitrosylation in health and disease: a current perspective.Regulation of Ryanodine Receptor Ion Channels Through Posttranslational Modifications.Detection of protein S-nitrosylation with the biotin-switch technique.sGC{alpha}1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes in calcium handling S-nitrosylation-regulated GPCR signaling.Targeted antioxidant treatment decreases cardiac alternans associated with chronic myocardial infarction Effect of sodium nitrite on ischaemia and reperfusion-induced arrhythmias in anaesthetized dogs: is protein S-nitrosylation involved?Nitric oxide signaling and the regulation of myocardial function.Dynamic denitrosylation via S-nitrosoglutathione reductase regulates cardiovascular function.Enzymatic mechanisms regulating protein S-nitrosylation: implications in health and disease.S-Nitrosylation of cardiac ion channels.Nitric Oxide Synthase 1 Modulates Basal and β-Adrenergic-Stimulated Contractility by Rapid and Reversible Redox-Dependent S-Nitrosylation of the Heart S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ.Effects of increased systolic Ca(2+) and β-adrenergic stimulation on Ca(2+) transient decline in NOS1 knockout cardiac myocytes.

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P2860

Deficient ryanodine receptor S-nitrosylation increases sarcoplasmic reticulum calcium leak and arrhythmogenesis in cardiomyocytes.

http://www.wikidata.org/entity/Q36300139

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2007 nî lūn-bûn

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2007年学术文章

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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type

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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Deficient ryanodine receptor S ...... thmogenesis in cardiomyocytes.

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Adriana V Treuer

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Daniel R Gonzalez

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Farideh Beigi

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Joshua M Hare

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P2860

Nitric oxide synthase in cardiac sarcoplasmic reticulum

The plasmamembrane calmodulin-dependent calcium pump: a major regulator of nitric oxide synthase I

A new generation of Ca2+ indicators with greatly improved fluorescence properties

FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death

Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia

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

Mechanisms of sudden cardiac death.

Cysteine-3635 is responsible for skeletal muscle ryanodine receptor modulation by NO

Abnormal intrastore calcium signaling in chronic heart failure.

A mathematical treatment of integrated Ca dynamics within the ventricular myocyte.

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20612-20617

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