Calsequestrin 2 deletion shortens the refractoriness of Ca²⁺ release and reduces rate-dependent Ca²⁺-alternans in intact mouse hearts.
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Calsequestrin 2 and arrhythmiasRole of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Calsequestrin mutations and catecholaminergic polymorphic ventricular tachycardiaCardiac electrophysiological imaging systems scalable for high-throughput drug testingStore-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling.Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death.Role of inositol 1,4,5-trisphosphate in the regulation of ventricular Ca(2+) signaling in intact mouse heart.Functional and structural characterization of a eurytolerant calsequestrin from the intertidal teleost Fundulus heteroclitus.Neuronal Na+ channel blockade suppresses arrhythmogenic diastolic Ca2+ release.Impaired calcium-calmodulin-dependent inactivation of Cav1.2 contributes to loss of sarcoplasmic reticulum calcium release refractoriness in mice lacking calsequestrin 2.Chasing cardiac physiology and pathology down the CaMKII cascadeRefractoriness of sarcoplasmic reticulum Ca2+ release determines Ca2+ alternans in atrial myocytesCalcium alternans in a couplon network model of ventricular myocytes: role of sarcoplasmic reticulum load.Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVTLocal Field Fluorescence Microscopy: Imaging Cellular Signals in Intact Hearts.Accelerated junctional rhythm and nonalternans repolarization lability precede ventricular tachycardia in Casq2-/- mice.Calcium alternans in cardiac myocytes: order from disorder.In silico prediction of drug therapy in catecholaminergic polymorphic ventricular tachycardia.Intact Heart Loose Patch Photolysis Reveals Ionic Current Kinetics During Ventricular Action PotentialsDecreased RyR2 refractoriness determines myocardial synchronization of aberrant Ca2+ release in a genetic model of arrhythmia.Neuronal Na+ Channels Are Integral Components of Pro-arrhythmic Na+/Ca2+ Signaling Nanodomain That Promotes Cardiac Arrhythmias During β-adrenergic Stimulation.A unified theory of calcium alternans in ventricular myocytes.Ca(2+)-activated chloride channel activity during Ca(2+) alternans in ventricular myocytes.Decoding myocardial Ca²⁺ signals across multiple spatial scales: a role for sensitivity analysis.The emerging role of calmodulin regulation of RyR2 in controlling heart rhythm, the progression of heart failure and the antiarrhythmic action of dantrolene.Evidence for a functional role of calsequestrin 2 in mouse atrium.Maximal acceleration of Ca2+ release refractoriness by β-adrenergic stimulation requires dual activation of kinases PKA and CaMKII in mouse ventricular myocytes.Sex-specific cardiovascular responses to control or high fat diet feeding in C57bl/6 mice chronically exposed to bisphenol A.Persistence of pro-arrhythmic spatio-temporal calcium patterns in atrial myocytes: a computational study of ping waves.Does the Goldilocks Principle apply to calcium release restitution in heart cells?R4496C RyR2 mutation impairs atrial and ventricular contractility.Roles of impaired intracellular calcium cycling in arrhythmogenicity of diabetic mouse model.Ambiguous interactions between diastolic and SR Ca2+ in the regulation of cardiac Ca2+ release.The role of luminal Ca regulation in Ca signaling refractoriness and cardiac arrhythmogenesis.Membrane potential determines calcium alternans through modulation of SR Ca2+ load and L-type Ca2+ current.Gene Transfer of Engineered Calmodulin Alleviates Ventricular Arrhythmias in a Calsequestrin-Associated Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia.Genetic variations involved in sudden cardiac death and their associations and interactions.Calcium-activated chloride current determines action potential morphology during calcium alternans in atrial myocytes.
P2860
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P2860
Calsequestrin 2 deletion shortens the refractoriness of Ca²⁺ release and reduces rate-dependent Ca²⁺-alternans in intact mouse hearts.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Calsequestrin 2 deletion short ...... ernans in intact mouse hearts.
@en
type
label
Calsequestrin 2 deletion short ...... ernans in intact mouse hearts.
@en
prefLabel
Calsequestrin 2 deletion short ...... ernans in intact mouse hearts.
@en
P2093
P2860
P1476
Calsequestrin 2 deletion short ...... ernans in intact mouse hearts.
@en
P2093
Ariel L Escobar
Azade D Petrosky
Bernardo Zepeda
Bjorn Knollmann
Dmytro Kornyeyev
Marcela Ferreiro
P2860
P356
10.1016/J.YJMCC.2011.09.020
P577
2011-09-29T00:00:00Z