Role of RyR2 phosphorylation in heart failure and arrhythmias: Controversies around ryanodine receptor phosphorylation in cardiac disease.
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Ongoing controversies surrounding cardiac remodeling: is it black and white-or rather fifty shades of gray?Compartmentalization role of A-kinase anchoring proteins (AKAPs) in mediating protein kinase A (PKA) signaling and cardiomyocyte hypertrophyMechanisms of ventricular arrhythmias: from molecular fluctuations to electrical turbulenceMechanisms of arrhythmogenesis related to calcium-driven alternans in a model of human atrial fibrillation.Loss of MD1 exacerbates pressure overload-induced left ventricular structural and electrical remodelling.Dantrolene suppresses spontaneous Ca2+ release without altering excitation-contraction coupling in cardiomyocytes of aged mice.Muscling in on the ryanodine receptor.Disrupted calcium release as a mechanism for atrial alternans associated with human atrial fibrillationA low-dose β1-blocker in combination with milrinone improves intracellular Ca2+ handling in failing cardiomyocytes by inhibition of milrinone-induced diastolic Ca2+ leakage from the sarcoplasmic reticulumAltered myocardial calcium cycling and energetics in heart failure--a rational approach for disease treatment.Computational analysis of the regulation of Ca(2+) dynamics in rat ventricular myocytesRecombinant Atrial Natriuretic Peptide Prevents Aberrant Ca2+ Leakage through the Ryanodine Receptor by Suppressing Mitochondrial Reactive Oxygen Species Production Induced by Isoproterenol in Failing Cardiomyocytes.Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing miceHuman G109E-inhibitor-1 impairs cardiac function and promotes arrhythmias.Calcium Sparks in the Heart: Dynamics and Regulation.Microtubule-Dependent Mitochondria Alignment Regulates Calcium Release in Response to Nanomechanical Stimulus in Heart Myocytes.Neuronal Na+ Channels Are Integral Components of Pro-arrhythmic Na+/Ca2+ Signaling Nanodomain That Promotes Cardiac Arrhythmias During β-adrenergic Stimulation.Pleiotropic Effects of Myocardial MMP-9 Inhibition to Prevent Ventricular Arrhythmia.mAKAP-a master scaffold for cardiac remodeling.Recent Developments in Heart Failure.Computational models of atrial cellular electrophysiology and calcium handling, and their role in atrial fibrillation.β-Adrenergic receptor stimulation inhibits proarrhythmic alternans in postinfarction border zone cardiomyocytes: a computational analysis.Serine/Threonine Phosphatases in Atrial Fibrillation.Cardiomyocyte Ca2+ homeostasis as a therapeutic target in heart failure with reduced and preserved ejection fraction.Regional distribution of T-tubule density in left and right atria in dogs.Calcium Signaling and Cardiac Arrhythmias.Investigational antiarrhythmic agents: promising drugs in early clinical development.Altered Mitochondrial Metabolism and Mechanosensation in the Failing Heart: Focus on Intracellular Calcium Signaling.Ablation of the cardiac ryanodine receptor phospho-site Ser2808 does not alter the adrenergic response or the progression to heart failure in mice. Elimination of the genetic background as critical variable.Maximal acceleration of Ca2+ release refractoriness by β-adrenergic stimulation requires dual activation of kinases PKA and CaMKII in mouse ventricular myocytes.Muscarinic Stimulation Facilitates Sarcoplasmic Reticulum Ca Release by Modulating Ryanodine Receptor 2 Phosphorylation Through Protein Kinase G and Ca/Calmodulin-Dependent Protein Kinase II.SPEG (Striated Muscle Preferentially Expressed Protein Kinase) Is Essential for Cardiac Function by Regulating Junctional Membrane Complex Activity.Roles of impaired intracellular calcium cycling in arrhythmogenicity of diabetic mouse model.Ion channels as part of macromolecular multiprotein complexes : Clinical significance.Cardiac RKIP induces a beneficial β-adrenoceptor-dependent positive inotropy.Force development and intracellular Ca2+ in intact cardiac muscles from gravin mutant mice.Calmodulin kinase II inhibition limits the pro-arrhythmic Ca2+ waves induced by cAMP-phosphodiesterase inhibitors.Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and CalciumCalcium in the Pathophysiology of Atrial Fibrillation and Heart FailureThe Subcellular Distribution of Ryanodine Receptors and L-Type Ca Channels Modulates Ca-Transient Properties and Spontaneous Ca-Release Events in Atrial Cardiomyocytes
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Role of RyR2 phosphorylation in heart failure and arrhythmias: Controversies around ryanodine receptor phosphorylation in cardiac disease.
description
2014 nî lūn-bûn
@nan
2014 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2014 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
name
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@ast
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@en
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@nl
type
label
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@ast
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@en
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@nl
prefLabel
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@ast
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@en
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@nl
P2860
P1433
P1476
Role of RyR2 phosphorylation i ...... horylation in cardiac disease.
@en
P2093
Dobromir Dobrev
P2860
P304
1311-9; discussion 1319
P356
10.1161/CIRCRESAHA.114.300568
P577
2014-04-01T00:00:00Z