Analyses of a novel SCN5A mutation (C1850S): conduction vs. repolarization disorder hypotheses in the Brugada syndrome.
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Mutations in sodium channel β-subunit SCN3B are associated with early-onset lone atrial fibrillationSolution NMR structure of Apo-calmodulin in complex with the IQ motif of human cardiac sodium channel NaV1.5Solution NMR structure of the C-terminal EF-hand domain of human cardiac sodium channel NaV1.5Distinct functional defect of three novel Brugada syndrome related cardiac sodium channel mutationsRe-evaluation of the action potential upstroke velocity as a measure of the Na+ current in cardiac myocytes at physiological conditions.Novel heterozygous mutation c.4282G>T in the SCN5A gene in a family with Brugada syndromeBasis for the Induction of Tissue-Level Phase-2 Reentry as a Repolarization Disorder in the Brugada SyndromeCharacterization of a novel Nav1.5 channel mutation, A551T, associated with Brugada syndrome.Using computational modeling to predict arrhythmogenesis and antiarrhythmic therapy.Cardiac channelopathies and sudden infant death syndrome.Arrhythmogenic right ventricular cardiomyopathy: considerations from in silico experiments.Investigations of the Navβ1b sodium channel subunit in human ventricle; functional characterization of the H162P Brugada syndrome mutant.Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation.Sinus Bradycardia in Carriers of the SCN5A-1795insD Mutation: Unraveling the Mechanism through Computer Simulations.The voltage-gated sodium channel EF-hands form an interaction with the III-IV linker that is disturbed by disease-causing mutations.Inhibition of Small Conductance Calcium-Activated Potassium (SK) Channels Prevents Arrhythmias in Rat Atria During β-Adrenergic and Muscarinic Receptor Activation.The Prevalence of Mutations inKCNQ1, KCNH2,andSCN5Ain an Unselected National Cohort of Young Sudden Unexplained Death CasesRegulation and physiological function of Nav1.5 and KCNQ1 channelsPredicting changes to I from missense mutations in human SCN5A
P2860
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P2860
Analyses of a novel SCN5A mutation (C1850S): conduction vs. repolarization disorder hypotheses in the Brugada syndrome.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Analyses of a novel SCN5A muta ...... heses in the Brugada syndrome.
@en
type
label
Analyses of a novel SCN5A muta ...... heses in the Brugada syndrome.
@en
prefLabel
Analyses of a novel SCN5A muta ...... heses in the Brugada syndrome.
@en
P2093
P2860
P50
P356
P1476
Analyses of a novel SCN5A muta ...... heses in the Brugada syndrome.
@en
P2093
Cora Corbaz
Dagmar I Keller
Etienne Pruvot
Jürg Schläpfer
Séverine Petitprez
P2860
P304
P356
10.1093/CVR/CVN023
P577
2008-02-05T00:00:00Z