Increased Ca2+ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia. - Wikidata - wikimedia - TriplyDB

Increased Ca2+ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia.

Increased Ca2+ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia.

http://www.wikidata.org/entity/Q33551271

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Molecular and genetic basis of sudden cardiac death A network-oriented perspective on cardiac calcium signaling Channel Activity of Cardiac Ryanodine Receptors (RyR2) Determines Potency and Efficacy of Flecainide and R-Propafenone against Arrhythmogenic Calcium Waves in Ventricular Cardiomyocytes Cardiac disease and arrhythmogenesis: Mechanistic insights from mouse models Inherited dysfunction of sarcoplasmic reticulum Ca2+ handling and arrhythmogenesis Phosphoinositide 3-kinase γ protects against catecholamine-induced ventricular arrhythmia through protein kinase A-mediated regulation of distinct phosphodiesterases A compartmentalized mathematical model of the β1-adrenergic signaling system in mouse ventricular myocytes Epac enhances excitation-transcription coupling in cardiac myocytes Urocortin induces positive inotropic effect in rat heart NOD1 activation induces cardiac dysfunction and modulates cardiac fibrosis and cardiomyocyte apoptosis RyRCa2+ leak limits cardiac Ca2+ window current overcoming the tonic effect of calmodulinin mice Catecholaminergic polymorphic ventricular tachycardia is caused by mutation-linked defective conformational regulation of the ryanodine receptor.Heterogeneity of ryanodine receptor dysfunction in a mouse model of catecholaminergic polymorphic ventricular tachycardia Targeting intracellular calcium cycling in catecholaminergic polymorphic ventricular tachycardia: a theoretical investigation.Paradoxical effect of increased diastolic Ca(2+) release and decreased sinoatrial node activity in a mouse model of catecholaminergic polymorphic ventricular tachycardia.Novel calmodulin mutations associated with congenital arrhythmia susceptibility.RyR2R420Q catecholaminergic polymorphic ventricular tachycardia mutation induces bradycardia by disturbing the coupled clock pacemaker mechanism.Purkinje cells from RyR2 mutant mice are highly arrhythmogenic but responsive to targeted therapy Robust anti-arrhythmic efficacy of verapamil and flunarizine against dofetilide-induced TdP arrhythmias is based upon a shared and a different mode of action.In situ confocal imaging in intact heart reveals stress-induced Ca(2+) release variability in a murine catecholaminergic polymorphic ventricular tachycardia model of type 2 ryanodine receptor(R4496C+/-) mutation The cardiac ryanodine receptor luminal Ca2+ sensor governs Ca2+ waves, ventricular tachyarrhythmias and cardiac hypertrophy in calsequestrin-null mice.A mathematical model of spontaneous calcium release in cardiac myocytes SERCA2a gene transfer decreases sarcoplasmic reticulum calcium leak and reduces ventricular arrhythmias in a model of chronic heart failure.Instabilities of the resting state in a mathematical model of calcium handling in cardiac myocytes.Abnormal termination of Ca2+ release is a common defect of RyR2 mutations associated with cardiomyopathies Reconciling depressed Ca2+ sparks occurrence with enhanced RyR2 activity in failing mice cardiomyocytes.Patient-Specific Human Induced Pluripotent Stem Cell Model Assessed with Electrical Pacing Validates S107 as a Potential Therapeutic Agent for Catecholaminergic Polymorphic Ventricular Tachycardia.Carvedilol analogue inhibits triggered activities evoked by both early and delayed afterdepolarizations High throughput measurement of Ca²⁺ dynamics for drug risk assessment in human stem cell-derived cardiomyocytes by kinetic image cytometry Gene mutations in cardiac arrhythmias: a review of recent evidence in ion channelopathies.Induced pluripotent stem cells in cardiovascular drug discovery.Ryanodine receptor mutations in arrhythmia: The continuing mystery of channel dysfunction.Ryanodine receptor studies using genetically engineered mice.Posttranslational modifications of cardiac ryanodine receptors: Ca(2+) signaling and EC-coupling.Regulation of RYR2 by sarcoplasmic reticulum Ca(2+).Biodegradable Polymeric Nanocapsules Prevent Cardiotoxicity of Anti-Trypanosomal Lychnopholide.NOD1 receptor is up-regulated in diabetic human and murine myocardium.Ca2+ signaling in human induced pluripotent stem cell-derived cardiomyocytes (iPS-CM) from normal and catecholaminergic polymorphic ventricular tachycardia (CPVT)-afflicted subjects.Ryanodine receptor gating controls generation of diastolic calcium waves in cardiac myocytes.The N-Terminal Region of the Ryanodine Receptor Affects Channel Activation.

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P2860

Increased Ca2+ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia.

http://www.wikidata.org/entity/Q33551271

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2008 nî lūn-bûn

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P2860

PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts

Identification of mutations in the cardiac ryanodine receptor gene in families affected with arrhythmogenic right ventricular cardiomyopathy type 2 (ARVD2)

Ryanodine receptor mutations associated with stress-induced ventricular tachycardia mediate increased calcium release in stimulated cardiomyocytes

Mutations of the cardiac ryanodine receptor (RyR2) gene in familial polymorphic ventricular tachycardia

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

Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia

A missense mutation in a highly conserved region of CASQ2 is associated with autosomal recessive catecholamine-induced polymorphic ventricular tachycardia in Bedouin families from Israel

Involvement of the cardiac ryanodine receptor/calcium release channel in catecholaminergic polymorphic ventricular tachycardia

Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle

RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR)

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