Enhanced store overload-induced Ca2+ release and channel sensitivity to luminal Ca2+ activation are common defects of RyR2 mutations linked to ventricular tachycardia and sudden death
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Removal of FKBP12.6 does not alter the conductance and activation of the cardiac ryanodine receptor or the susceptibility to stress-induced ventricular arrhythmiasProtein protein interactions between triadin and calsequestrin are involved in modulation of sarcoplasmic reticulum calcium release in cardiac myocytesK201 (JTV519) suppresses spontaneous Ca2+ release and [3H]ryanodine binding to RyR2 irrespective of FKBP12.6 associationTMEM43 mutation p.S358L alters intercalated disc protein expression and reduces conduction velocity in arrhythmogenic right ventricular cardiomyopathyCardiac ryanodine receptors control heart rate and rhythmicity in adult miceCa2+ stores regulate ryanodine receptor Ca2+ release channels via luminal and cytosolic Ca2+ sitesDefective domain-domain interactions within the ryanodine receptor as a critical cause of diastolic Ca2+ leak in failing heartsInherited dysfunction of sarcoplasmic reticulum Ca2+ handling and arrhythmogenesisExome Analyses of Long QT Syndrome Reveal Candidate Pathogenic Mutations in Calmodulin-Interacting GenesDirect association of the reticulon protein RTN1A with the ryanodine receptor 2 in neuronsCasq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardiaCalmodulin kinase II-mediated sarcoplasmic reticulum Ca2+ leak promotes atrial fibrillation in mice.Heterogeneity of ryanodine receptor dysfunction in a mouse model of catecholaminergic polymorphic ventricular tachycardiaLeaky RyR2 channels unleash a brainstem spreading depolarization mechanism of sudden cardiac death.The molecular basis of catecholaminergic polymorphic ventricular tachycardia: what are the different hypotheses regarding mechanisms?Search for cardiac calcium cycling gene mutations in familial ventricular arrhythmias resembling catecholaminergic polymorphic ventricular tachycardia.Characterization of a novel mutation in the cardiac ryanodine receptor that results in catecholaminergic polymorphic ventricular tachycardiaRecent developments in the management of patients at risk for sudden cardiac death.The role of ion channelopathies in sudden cardiac death: implications for clinical practice.Dysregulated sarcoplasmic reticulum calcium release: potential pharmacological target in cardiac disease.Role of RyR2 phosphorylation in heart failure and arrhythmias: Controversies around ryanodine receptor phosphorylation in cardiac disease.Localization of an NH(2)-terminal disease-causing mutation hot spot to the "clamp" region in the three-dimensional structure of the cardiac ryanodine receptor.Ryanodine receptor channelopathies.RNA-binding protein RBM20 represses splicing to orchestrate cardiac pre-mRNA processing.Cardiac ryanodine receptor phosphorylation: target sites and functional consequencesInhibition of cardiac Ca2+ release channels (RyR2) determines efficacy of class I antiarrhythmic drugs in catecholaminergic polymorphic ventricular tachycardia.Sudden cardiac death and inherited channelopathy: the basic electrophysiology of the myocyte and myocardium in ion channel disease.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+/-) mutationDefects in T-tubular electrical activity underlie local alterations of calcium release in heart failureThe ryanodine receptor in cardiac physiology and disease.The ryanodine receptor store-sensing gate controls Ca2+ waves and Ca2+-triggered arrhythmiasSuperresolution modeling of calcium release in the heartLocalization of the dantrolene-binding sequence near the FK506-binding protein-binding site in the three-dimensional structure of the ryanodine receptor.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 myocytesMice with the R176Q cardiac ryanodine receptor mutation exhibit catecholamine-induced ventricular tachycardia and cardiomyopathy.SERCA2a gene transfer decreases sarcoplasmic reticulum calcium leak and reduces ventricular arrhythmias in a model of chronic heart failure.Calcium and arrhythmogenesis.Enhanced ER Ca2+ store filling by overexpression of SERCA2b promotes IP3-evoked puffs.Endoplasmic reticulum Ca(2+) handling in excitable cells in health and disease
P2860
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P2860
Enhanced store overload-induced Ca2+ release and channel sensitivity to luminal Ca2+ activation are common defects of RyR2 mutations linked to ventricular tachycardia and sudden death
description
2005 nî lūn-bûn
@nan
2005 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2005年の論文
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2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Enhanced store overload-induce ...... r tachycardia and sudden death
@ast
Enhanced store overload-induce ...... r tachycardia and sudden death
@en
Enhanced store overload-induce ...... r tachycardia and sudden death
@nl
type
label
Enhanced store overload-induce ...... r tachycardia and sudden death
@ast
Enhanced store overload-induce ...... r tachycardia and sudden death
@en
Enhanced store overload-induce ...... r tachycardia and sudden death
@nl
prefLabel
Enhanced store overload-induce ...... r tachycardia and sudden death
@ast
Enhanced store overload-induce ...... r tachycardia and sudden death
@en
Enhanced store overload-induce ...... r tachycardia and sudden death
@nl
P2093
P3181
P1433
P1476
Enhanced store overload-induce ...... r tachycardia and sudden death
@en
P2093
Bailong Xiao
Dawei Jiang
Donald J Hunt
Huihui Kong
Philip Choi
Ruiwu Wang
S R Wayne Chen
P304
P3181
P356
10.1161/01.RES.0000192146.85173.4B
P407
P577
2005-11-25T00:00:00Z