Enhanced ryanodine receptor-mediated calcium leak determines reduced sarcoplasmic reticulum calcium content in chronic canine heart failure. - Wikidata - wikimedia - TriplyDB

Enhanced ryanodine receptor-mediated calcium leak determines reduced sarcoplasmic reticulum calcium content in chronic canine heart failure.

Enhanced ryanodine receptor-mediated calcium leak determines reduced sarcoplasmic reticulum calcium content in chronic canine heart failure.

http://www.wikidata.org/entity/Q36156470

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Dysfunctional ryanodine receptors in the heart: new insights into complex cardiovascular diseases 'Ryanopathy': causes and manifestations of RyR2 dysfunction in heart failure Dysregulated sarcoplasmic reticulum calcium release: potential pharmacological target in cardiac disease.Redox-mediated reciprocal regulation of SERCA and Na+-Ca2+ exchanger contributes to sarcoplasmic reticulum Ca2+ depletion in cardiac myocytes.Late sodium current contributes to diastolic cell Ca2+ accumulation in chronic heart failure.Epac2 mediates cardiac β1-adrenergic-dependent sarcoplasmic reticulum Ca2+ leak and arrhythmia.The relationship between arrhythmogenesis and impaired contractility in heart failure: role of altered ryanodine receptor function.Impaired calcium-calmodulin-dependent inactivation of Cav1.2 contributes to loss of sarcoplasmic reticulum calcium release refractoriness in mice lacking calsequestrin 2.Dissociation of Calcium Transients and Force Development following a Change in Stimulation Frequency in Isolated Rabbit Myocardium Dantrolene prevents arrhythmogenic Ca2+ release in heart failure Refractoriness of sarcoplasmic reticulum Ca2+ release determines Ca2+ alternans in atrial myocytes Cellular mechanisms of arrhythmogenic cardiac alternans.Myofilament calcium de-sensitization and contractile uncoupling prevent pause-triggered ventricular tachycardia in mouse hearts with chronic myocardial infarction Revealing the cellular basis of heart failure Partial downregulation of junctin enhances cardiac calcium cycling without eliciting ventricular arrhythmias in mice.Ryanodine receptor-mediated arrhythmias and sudden cardiac death.Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death.Ca handling during excitation-contraction coupling in heart failure.The SR-mitochondria interaction: a new player in cardiac pathophysiology.Novel therapeutic targets for the treatment of heart failure.The Significance of the Late Na+ Current for Arrhythmia Induction and the Therapeutic Antiarrhythmic Potential of Ranolazine.Biphasic decay of the Ca transient results from increased sarcoplasmic reticulum Ca leak.Calcium and Excitation-Contraction Coupling in the Heart Redox modification of ryanodine receptors contributes to sarcoplasmic reticulum Ca2+ leak in chronic heart failure.NOD1, a new player in cardiac function and calcium handling.Systolic [Ca2+ ]i regulates diastolic levels in rat ventricular myocytes.Frequency and release flux of calcium sparks in rat cardiac myocytes: a relation to RYR gating.Function of the CaMKII-ryanodine receptor signaling pathway in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia.Luminal Ca2+ controls activation of the cardiac ryanodine receptor by ATP.Ca²+-dependent phosphorylation of RyR2 can uncouple channel gating from direct cytosolic Ca²+ regulation.Muscarinic Stimulation Facilitates Sarcoplasmic Reticulum Ca Release by Modulating Ryanodine Receptor 2 Phosphorylation Through Protein Kinase G and Ca/Calmodulin-Dependent Protein Kinase II.A small leak may sink a great ship but what does it do to the heart?Ca²+ spark-dependent and -independent sarcoplasmic reticulum Ca²+ leak in normal and failing rabbit ventricular myocytes.R4496C RyR2 mutation impairs atrial and ventricular contractility.Alteration of sarcoplasmic reticulum Ca2+ release termination by ryanodine receptor sensitization and in heart failure.Local energetic regulation of sarcoplasmic and myosin ATPase is differently impaired in rats with heart failure.Ups and downs of calcium in the heart.The role of luminal Ca regulation in Ca signaling refractoriness and cardiac arrhythmogenesis.The role of spatial organization of Ca2+ release sites in the generation of arrhythmogenic diastolic Ca2+ release in myocytes from failing hearts.Regulation of sarcoplasmic reticulum Ca²⁺ leak by cytosolic Ca²⁺ in rabbit ventricular myocytes.

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Enhanced ryanodine receptor-mediated calcium leak determines reduced sarcoplasmic reticulum calcium content in chronic canine heart failure.

http://www.wikidata.org/entity/Q36156470

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Enhanced ryanodine receptor-me ...... chronic canine heart failure.

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Enhanced ryanodine receptor-me ...... chronic canine heart failure.

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Enhanced ryanodine receptor-me ...... chronic canine heart failure.

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Andriy Belevych

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Cynthia A Carnes

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Dmitry Terentyev

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Robert L Hamlin

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Sandor Györke

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Zuzana Kubalova

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P2860

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

Clinical phenotype and functional characterization of CASQ2 mutations associated with catecholaminergic polymorphic ventricular tachycardia

The role of calsequestrin, triadin, and junctin in conferring cardiac ryanodine receptor responsiveness to luminal calcium.

Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation-contraction coupling in the heart

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

Complex formation between junctin, triadin, calsequestrin, and the ryanodine receptor. Proteins of the cardiac junctional sarcoplasmic reticulum membrane

Dynamic regulation of sarcoplasmic reticulum Ca(2+) content and release by luminal Ca(2+)-sensitive leak in rat ventricular myocytes.

Abnormal intrastore calcium signaling in chronic heart failure.

Termination of cardiac Ca(2+) sparks: an investigative mathematical model of calcium-induced calcium release

Differential regulation of two types of intracellular calcium release channels during end-stage heart failure

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