Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels - Wikidata - awgldk - TriplyDB

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

http://www.wikidata.org/entity/Q35157593

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RBM20, a gene for hereditary cardiomyopathy, regulates titin splicing Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sites Cell membrane expression of cardiac sodium channel Na(v)1.5 is modulated by alpha-actinin-2 interaction Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation-contraction coupling in the heart Na⁺ transport in the normal and failing heart - remember the balance Recent advances in understanding cardiac contractility in health and disease Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions-A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases Ca(2+) signaling in the myocardium by (redox) regulation of PKA/CaMKII The role of late I Na in development of cardiac arrhythmias Ion Channels in the Heart Transcriptional pathways and potential therapeutic targets in the regulation of Ncx1 expression in cardiac hypertrophy and failure Regulation of intracellular Na(+) in health and disease: pathophysiological mechanisms and implications for treatment CaMKII regulation of cardiac K channels The late Na+ current--origin and pathophysiological relevance CaMKII-dependent regulation of cardiac Na(+) homeostasis Calmodulin-dependent protein kinase II: linking heart failure and arrhythmias Na+ channel function, regulation, structure, trafficking and sequestration New treatment options for late Na current, arrhythmias, and diastolic dysfunction Mechanisms of altered Ca²⁺ handling in heart failure Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences New therapeutic targets in cardiology: arrhythmias and Ca2+/calmodulin-dependent kinase II (CaMKII)CaMKIIdelta subtypes: localization and function Targets for therapy in sarcomeric cardiomyopathies Calcium dysregulation in atrial fibrillation: the role of CaMKII Generation of highly purified human cardiomyocytes from peripheral blood mononuclear cell-derived induced pluripotent stem cells Late Na(+) current and protracted electrical recovery are critical determinants of the aging myopathy Aberrant sodium influx causes cardiomyopathy and atrial fibrillation in mice Role of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Perspective: a dynamics-based classification of ventricular arrhythmias Post-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmias Simulation of the undiseased human cardiac ventricular action potential: model formulation and experimental validation A β(IV)-spectrin/CaMKII signaling complex is essential for membrane excitability in mice Location matters: clarifying the concept of nuclear and cytosolic CaMKII subtypes Calmodulin binding proteins provide domains of local Ca2+ signaling in cardiac myocytes Synergy between CaMKII substrates and β-adrenergic signaling in regulation of cardiac myocyte Ca(2+) handling.Diastolic dysfunction and heart failure with a preserved ejection fraction: Relevance in critical illness and anaesthesia Voltage-Gated Sodium Channel Phosphorylation at Ser571 Regulates Late Current, Arrhythmia, and Cardiac Function In Vivo.Oxidized calmodulin kinase II regulates conduction following myocardial infarction: a computational analysis.

P2860

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P2860

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

http://www.wikidata.org/entity/Q35157593

description

2006 nî lūn-bûn

@nan

2006 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի նոյեմբերին հրատարակված գիտական հոդված

@hy

2006年の論文

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2006年論文

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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

name

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

@ast

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

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type

label

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

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Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

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prefLabel

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

@ast

Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

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Journal of Clinical Investigation

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Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels

@en

P2093

Claudius Jacobshagen

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Eva C L Rasenack

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Joan Heller Brown

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Lars S Maier

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Nataliya Dybkova

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Sebastian K G Maier

http://www.w3.org/2001/XMLSchema#string

Stefan Wagner

http://www.w3.org/2001/XMLSchema#string

Tong Zhang

http://www.w3.org/2001/XMLSchema#string

P2860

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

A calcium sensor in the sodium channel modulates cardiac excitability

Transgenic CaMKIIdeltaC overexpression uniquely alters cardiac myocyte Ca2+ handling: reduced SR Ca2+ load and activated SR Ca2+ release

The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure

A single Na(+) channel mutation causing both long-QT and Brugada syndromes

Identification and expression of delta-isoforms of the multifunctional Ca2+/calmodulin-dependent protein kinase in failing and nonfailing human myocardium

The steady state TTX-sensitive ("window") sodium current in cardiac Purkinje fibres

Novel, ultraslow inactivating sodium current in human ventricular cardiomyocytes

Molecular mechanism for an inherited cardiac arrhythmia.

Na(+)-Ca(2+) exchanger overexpression predisposes to reactive oxygen species-induced injury.

P304

3127-3138

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scholarly article

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10.1172/JCI26620

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P407

P433

12

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P478

116

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Paulus Kirchhof

Larissa Fabritz

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2006-11-22T00:00:00Z

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6672760

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17124532

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1654201

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