The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.
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Computer-based prediction of the drug proarrhythmic effect: problems, issues, known and suspected challengesScreening for acute IKr block is insufficient to detect torsades de pointes liability: role of late sodium current.Substituted N-(biphenyl-4'-yl)methyl (R)-2-acetamido-3-methoxypropionamides: potent anticonvulsants that affect frequency (use) dependence and slow inactivation of sodium channels.Deletion of PDK1 causes cardiac sodium current reduction in miceCardiac sodium channel palmitoylation regulates channel availability and myocyte excitability with implications for arrhythmia generationMolecular Pathophysiology of Congenital Long QT Syndrome.Changes in cardiac Nav1.5 expression, function, and acetylation by pan-histone deacetylase inhibitors.Cardiac channelopathies associated with infantile fatal ventricular arrhythmias: from the cradle to the bench.Toward a Reasoned Classification of Diseases Using Physico-Chemical Based Phenotypes.
P2860
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P2860
The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.
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2012 nî lūn-bûn
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2012年の論文
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2012年学术文章
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The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@en
The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@nl
type
label
The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@en
The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@nl
prefLabel
The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@en
The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@nl
P2093
P2860
P1476
The human Nav1.5 F1486 deletio ...... reduced lidocaine sensitivity.
@en
P2093
Andrew D Piekarz
Andy Hudmon
Hanying Chen
Nicole M Ashpole
Theodore R Cummins
Weihua Song
Weinian Shou
Yucheng Xiao
P2860
P304
P356
10.1113/JPHYSIOL.2012.235374
P407
P577
2012-07-23T00:00:00Z