Ser-2030, but not Ser-2808, is the major phosphorylation site in cardiac ryanodine receptors responding to protein kinase A activation upon beta-adrenergic stimulation in normal and failing hearts.
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Phosphodiesterase 4D regulates baseline sarcoplasmic reticulum Ca2+ release and cardiac contractility, independently of L-type Ca2+ currentCounteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases'Ryanopathy': causes and manifestations of RyR2 dysfunction in heart failureA compartmentalized mathematical model of the β1-adrenergic signaling system in mouse ventricular myocytesPhosphorylation of the cAMP-dependent protein kinase (PKA) regulatory subunit modulates PKA-AKAP interaction, substrate phosphorylation, and calcium signaling in cardiac cellsEffects of therapy using the Celacade system on structural and functional cardiac remodelling in rats following myocardial infarction.Pivotal effects of phosphodiesterase inhibitors on myocyte contractility and viability in normal and ischemic hearts.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.CaMKII regulation of cardiac ryanodine receptors and inositol triphosphate receptors.Protein Kinases as Drug Development Targets for Heart Disease TherapyShortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death.Cardiac ryanodine receptor phosphorylation: target sites and functional consequencesRyanodine receptors: structure, expression, molecular details, and function in calcium release.MicroRNA-1 and -133 increase arrhythmogenesis in heart failure by dissociating phosphatase activity from RyR2 complex.Dantrolene suppresses spontaneous Ca2+ release without altering excitation-contraction coupling in cardiomyocytes of aged mice.SR-targeted CaMKII inhibition improves SR Ca²+ handling, but accelerates cardiac remodeling in mice overexpressing CaMKIIδC.ß-Adrenergic stimulation increases RyR2 activity via intracellular Ca2+ and Mg2+ regulationEpac activation, altered calcium homeostasis and ventricular arrhythmogenesis in the murine heart.A 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 reticulumRegulation of Ryanodine Receptor Ion Channels Through Posttranslational Modifications.β-Adrenergic receptor stimulation and activation of protein kinase A protect against α1-adrenergic-mediated phosphorylation of protein kinase D and histone deacetylase 5Skeletal and cardiac ryanodine receptors exhibit different responses to Ca2+ overload and luminal ca2+.Ca2+/calmodulin kinase II increases ryanodine binding and Ca2+-induced sarcoplasmic reticulum Ca2+ release kinetics during beta-adrenergic stimulation.Phosphodiesterase-4 blunts inotropism and arrhythmias but not sinoatrial tachycardia of (-)-adrenaline mediated through mouse cardiac beta(1)-adrenoceptors.Arrhythmogenic ion-channel remodeling in the heart: heart failure, myocardial infarction, and atrial fibrillation.Altered sarcoplasmic reticulum calcium cycling--targets for heart failure therapy.PKA phosphorylation of cardiac ryanodine receptor modulates SR luminal Ca2+ sensitivity.Ryanodine receptor phosphorylation at Serine 2030, 2808 and 2814 in rat cardiomyocytes.Calcium/calmodulin-dependent kinase II and nitric oxide synthase 1-dependent modulation of ryanodine receptors during β-adrenergic stimulation is restricted to the dyadic cleftSpontaneous calcium release in tissue from the failing canine heart.Localization of PKA phosphorylation site, Ser(2030), in the three-dimensional structure of cardiac ryanodine receptor.Ryanodine receptor mutations in arrhythmia: The continuing mystery of channel dysfunction.The structural biology of ryanodine receptors.Ryanodine receptors: structure and function.Anchored protein kinase A signalling in cardiac cellular electrophysiology.Regulation of Ca(2+) transient by PP2A in normal and failing heart.Bcl-2 and FKBP12 bind to IP3 and ryanodine receptors at overlapping sites: the complexity of protein-protein interactions for channel regulation.The ryanodine receptor provides high throughput Ca2+-release but is precisely regulated by networks of associated proteins: a focus on proteins relevant to phosphorylation.ARVC-related mutations in divergent region 3 alter functional properties of the cardiac ryanodine receptor.
P2860
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P2860
Ser-2030, but not Ser-2808, is the major phosphorylation site in cardiac ryanodine receptors responding to protein kinase A activation upon beta-adrenergic stimulation in normal and failing hearts.
description
2006 nî lūn-bûn
@nan
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
2006年论文
@zh
2006年论文
@zh-cn
name
Ser-2030, but not Ser-2808, is ...... in normal and failing hearts.
@en
type
label
Ser-2030, but not Ser-2808, is ...... in normal and failing hearts.
@en
prefLabel
Ser-2030, but not Ser-2808, is ...... in normal and failing hearts.
@en
P2093
P2860
P356
P1433
P1476
Ser-2030, but not Ser-2808, is ...... n in normal and failing hearts
@en
P2093
Bailong Xiao
Dongmei Yang
Guofeng Zhong
Henk Ter Keurs
Heping Cheng
Keyun Chen
Michael P Walsh
S R Wayne Chen
Yakhin Shimoni
P2860
P356
10.1042/BJ20060116
P407
P577
2006-05-01T00:00:00Z