Late Na+ current produced by human cardiac Na+ channel isoform Nav1.5 is modulated by its beta1 subunit.
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Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sitesThe role of late I Na in development of cardiac arrhythmiasChannelopathies from mutations in the cardiac sodium channel protein complexCaMKII-dependent regulation of cardiac Na(+) homeostasisDesmosomes and the sodium channel complex: implications for arrhythmogenic cardiomyopathy and Brugada syndromePost-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmiasComparison of electrophysiological data from human-induced pluripotent stem cell-derived cardiomyocytes to functional preclinical safety assays.miR-19b Regulates Ventricular Action Potential Duration in Zebrafish.Inhibition of serum and glucocorticoid regulated kinase-1 as novel therapy for cardiac arrhythmia disordersModeling Inherited Arrhythmia Disorders Using Induced Pluripotent Stem Cell-Derived Cardiomyocytes.Diseases caused by mutations in Nav1.5 interacting proteinsPost-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure.Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5.Functional features of trans-differentiated hair cells mediated by Atoh1 reveals a primordial mechanism.Pathophysiology of the cardiac late Na current and its potential as a drug target.A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine.Cardiac calmodulin kinase: a potential target for drug design.Late sodium current: A mechanism for angina, heart failure, and arrhythmia.The late sodium current in heart failure: pathophysiology and clinical relevance.Mechanisms of noncovalent β subunit regulation of NaV channel gating.Reactive oxygen species-activated Ca/calmodulin kinase IIδ is required for late I(Na) augmentation leading to cellular Na and Ca overload.Contribution of sodium channel neuronal isoform Nav1.1 to late sodium current in ventricular myocytes from failing hearts.Variants: Association With Cardiac Disorders
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P2860
Late Na+ current produced by human cardiac Na+ channel isoform Nav1.5 is modulated by its beta1 subunit.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 03 March 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Late Na+ current produced by h ...... odulated by its beta1 subunit.
@en
Late Na+ current produced by h ...... odulated by its beta1 subunit.
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type
label
Late Na+ current produced by h ...... odulated by its beta1 subunit.
@en
Late Na+ current produced by h ...... odulated by its beta1 subunit.
@nl
prefLabel
Late Na+ current produced by h ...... odulated by its beta1 subunit.
@en
Late Na+ current produced by h ...... odulated by its beta1 subunit.
@nl
P2860
P1476
Late Na+ current produced by h ...... modulated by its beta1 subunit
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P2093
Albertas Undrovinas
John W Kyle
P2860
P2888
P304
P356
10.1007/S12576-009-0029-7
P577
2009-03-03T00:00:00Z