NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
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Regulation of CaMKII signaling in cardiovascular diseaseCa(2+) signaling in the myocardium by (redox) regulation of PKA/CaMKIIThe emerging role of CaMKII in cancerCaMKII oxidative activation and the pathogenesis of cardiac diseaseCa(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequencesCalcium dysregulation in atrial fibrillation: the role of CaMKIIRole of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Nitric oxide induces Ca2+-independent activity of the Ca2+/calmodulin-dependent protein kinase II (CaMKII).Nitric oxide-dependent activation of CaMKII increases diastolic sarcoplasmic reticulum calcium release in cardiac myocytes in response to adrenergic stimulation.Chasing cardiac physiology and pathology down the CaMKII cascadeS-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ.Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signalCalcium/calmodulin-dependent kinase II and nitric oxide synthase 1-dependent modulation of ryanodine receptors during β-adrenergic stimulation is restricted to the dyadic cleftOxidant stress promotes disease by activating CaMKII.CaMKII in sinoatrial node physiology and dysfunction.CaMKII inhibitors: from research tools to therapeutic agentsMechanisms of CaMKII Activation in the Heart.Ca(2+) /calmodulin dependent kinase II: a critical mediator in determining reperfusion outcomes in the heart?CaMKIIδ and cardiomyocyte Ca(2+) signalling new perspectives on splice variant targeting.Nitric oxide: what's new to NO?CaMKII is a nodal signal for multiple programmed cell death pathways in heart.Inducible cardiomyocyte-specific deletion of CaM kinase II protects from pressure overload-induced heart failure.The Golgi apparatus is a functionally distinct Ca2+ store regulated by the PKA and Epac branches of the β1-adrenergic signaling pathway.Molecular and cellular neurocardiology: development, and cellular and molecular adaptations to heart disease.Maximal acceleration of Ca2+ release refractoriness by β-adrenergic stimulation requires dual activation of kinases PKA and CaMKII in mouse ventricular myocytes.Mechano-chemo transduction tunes the heartstrings.Reversible redox modifications of ryanodine receptor ameliorate ventricular arrhythmias in the ischemic-reperfused heart.Inhibition of cardiac CaMKII to cure heart failure: step by step towards translation?Adrenergic Fight-or-Flight: S-NO Falls on PKA Targets.β-Adrenergic induced SR Ca2+ leak is mediated by an Epac-NOS pathway.Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium
P2860
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P2860
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
description
2013 nî lūn-bûn
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2013年の論文
@ja
2013年学术文章
@wuu
2013年学术文章
@zh
2013年学术文章
@zh-cn
2013年学术文章
@zh-hans
2013年学术文章
@zh-my
2013年学术文章
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2013年學術文章
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2013年學術文章
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name
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
@en
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
@nl
type
label
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
@en
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
@nl
prefLabel
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
@en
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle.
@nl
P2860
P356
P1476
NO-dependent CaMKII activation during β-adrenergic stimulation of cardiac muscle
@en
P2093
Daniel A Gutierrez
Jakob Ogrodnik
P2860
P304
P356
10.1093/CVR/CVT201
P577
2013-08-20T00:00:00Z