Clinical phenotype and functional characterization of CASQ2 mutations associated with catecholaminergic polymorphic ventricular tachycardia
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Role of Junctin protein interactions in cellular dynamics of calsequestrin polymer upon calcium perturbationCalsequestrin 2 and arrhythmiasFlecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humansHuman Induced Pluripotent Stem Cell-Derived Cardiomyocytes Afford New Opportunities in Inherited Cardiovascular Disease ModelingGenetics of inherited primary arrhythmia disordersPernicious attrition and inter-RyR2 CICR current control in cardiac muscleClinical Potentials of Cardiomyocytes Derived from Patient-Specific Induced Pluripotent Stem CellsCalsequestrin 2 (CASQ2) mutations increase expression of calreticulin and ryanodine receptors, causing catecholaminergic polymorphic ventricular tachycardiaCalsequestrin mutations and catecholaminergic polymorphic ventricular tachycardiaInherited dysfunction of sarcoplasmic reticulum Ca2+ handling and arrhythmogenesisThe catecholaminergic polymorphic ventricular tachycardia mutation R33Q disrupts the N-terminal structural motif that regulates reversible calsequestrin polymerizationThe calsequestrin mutation CASQ2D307H does not affect protein stability and targeting to the junctional sarcoplasmic reticulum but compromises its dynamic regulation of calcium bufferingPrevention of ventricular arrhythmia and calcium dysregulation in a catecholaminergic polymorphic ventricular tachycardia mouse model carrying calsequestrin-2 mutation.Therapeutic approach for patients with catecholaminergic polymorphic ventricular tachycardia: state of the art and future developments.Catecholaminergic polymorphic ventricular tachycardia in a patient with recurrent exertional syncopeCardiac syncope.Effects of flecainide on exercise-induced ventricular arrhythmias and recurrences in genotype-negative patients with catecholaminergic polymorphic ventricular tachycardia.Modeling Catecholaminergic Polymorphic Ventricular Tachycardia using Induced Pluripotent Stem Cell-derived Cardiomyocytes.Optimizing catecholaminergic polymorphic ventricular tachycardia therapy in calsequestrin-mutant miceSubcellular Ca2+ signaling in the heart: the role of ryanodine receptor sensitivity.Calcium handling in zebrafish ventricular myocytes.Genetics of sudden cardiac death.Flecainide therapy reduces exercise-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardiaThe cardiac ryanodine receptor luminal Ca2+ sensor governs Ca2+ waves, ventricular tachyarrhythmias and cardiac hypertrophy in calsequestrin-null mice.Calcium and arrhythmogenesis.Calcium/calmodulin-dependent protein kinase II (CaMKII) inhibition ameliorates arrhythmias elicited by junctin ablation under stress conditionsChain-reaction Ca(2+) signaling in the heart.Enhanced ryanodine receptor-mediated calcium leak determines reduced sarcoplasmic reticulum calcium content in chronic canine heart failure.Patient-Specific Human Induced Pluripotent Stem Cell Model Assessed with Electrical Pacing Validates S107 as a Potential Therapeutic Agent for Catecholaminergic Polymorphic Ventricular Tachycardia.Luminal Ca2+ regulation of single cardiac ryanodine receptors: insights provided by calsequestrin and its mutantsModulation of SR Ca release by luminal Ca and calsequestrin in cardiac myocytes: effects of CASQ2 mutations linked to sudden cardiac death.Molecular and electrophysiological bases of catecholaminergic polymorphic ventricular tachycardia.Decreased RyR2 refractoriness determines myocardial synchronization of aberrant Ca2+ release in a genetic model of arrhythmia.Regulatory roles of junctin in sarcoplasmic reticulum calcium cycling and myocardial function.Mechanisms and potential therapeutic targets for ventricular arrhythmias associated with impaired cardiac calcium cycling.Mechanism of calsequestrin regulation of single cardiac ryanodine receptor in normal and pathological conditions.Altered Ca2+ sparks in aging skeletal and cardiac muscle.Timing in cellular Ca2+ signalingA mutation in calsequestrin, CASQ2D307H, impairs Sarcoplasmic Reticulum Ca2+ handling and causes complex ventricular arrhythmias in mice.Cardiomyocytes generated from CPVTD307H patients are arrhythmogenic in response to β-adrenergic stimulation.
P2860
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P2860
Clinical phenotype and functional characterization of CASQ2 mutations associated with catecholaminergic polymorphic ventricular tachycardia
description
2006 nî lūn-bûn
@nan
2006 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Clinical phenotype and functio ...... orphic ventricular tachycardia
@ast
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en-gb
Clinical phenotype and functio ...... orphic ventricular tachycardia
@nl
type
label
Clinical phenotype and functio ...... orphic ventricular tachycardia
@ast
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en-gb
Clinical phenotype and functio ...... orphic ventricular tachycardia
@nl
prefLabel
Clinical phenotype and functio ...... orphic ventricular tachycardia
@ast
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en-gb
Clinical phenotype and functio ...... orphic ventricular tachycardia
@nl
P2093
P921
P3181
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P1476
Clinical phenotype and functio ...... orphic ventricular tachycardia
@en
P2093
Alessandra Nori
Carlo Napolitano
Dmitry Terentyev
Federica Turcato
Giorgia Valle
Marina Raffaele di Barletta
Mirella Memmi
Nicoletta Rizzi
Pompeo Volpe
Sandor Gyorke
P304
P3181
P356
10.1161/CIRCULATIONAHA.106.623793
P407
P577
2006-09-05T00:00:00Z