SCN5A channelopathies – An update on mutations and mechanisms
Author:
Publisher
Elsevier BV
Subject
Molecular Biology,Biophysics
Reference196 articles.
1. Regulation of the voltage-gated cardiac sodium channel Nav1.5 by interacting proteins;Abriel;Trends Cardiovasc. Med.,2005
2. Novel arrhythmogenic mechanism revealed by a long-QT syndrome mutation in the cardiac Na+ channel;Abriel;Circ. Res.,2001
3. Postmortem molecular analysis of SCN5A defects in sudden infant death syndrome;Ackerman;JAMA,2001
4. Spectrum and prevalence of cardiac sodium channel variants among black, white, Asian, and Hispanic individuals: implications for arrhythmogenic susceptibility and Brugada/long QT syndrome genetic testing;Ackerman;Heart Rhythm,2004
5. A novel SCN5A mutation associated with idiopathic ventricular fibrillation without typical ECG findings of Brugada syndrome;Akai;FEBS Lett.,2000
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1. Systematic analysis of SCN5A variants associated with inherited cardiac diseases;Heart Rhythm;2024-08
2. "Re-evaluation of variants of uncertain significance in patients with hereditary arrhythmogenic disorders";BMC Cardiovascular Disorders;2024-07-27
3. Requirement of β subunit for the reduced voltage-gated Na+ current of a Brugada syndrome patient having novel double missense mutation (p.A385T/R504T) of SCN5A;The Korean Journal of Physiology & Pharmacology;2024-07-01
4. Variability in reported midpoints of (in)activation of cardiac INa;2024-05-12
5. Biophysical mechanisms of myocardium sodium channelopathies;Pflügers Archiv - European Journal of Physiology;2024-03-01
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