Associated Papers
Prevalence and relevance of H558R in the efficacy and toxicity of flecainide in patients with atrial fibrillation: a cohort study.
Trincado Ave M et al.
Heart (british Cardiac Society), 2025
Genetic Characteristics and Transcriptional Regulation of Sodium Channel Related Genes in Chinese Patients With Brugada Syndrome.
Zhang Z et al.
Frontiers in Cardiovascular Medicine, 2021
Life Cycle of the Cardiac Voltage-Gated Sodium Channel NaV1.5.
Dong C et al.
Frontiers in Physiology, 2020
Further Insights in the Most Common SCN5A Mutation Causing Overlapping Phenotype of Long QT Syndrome, Brugada Syndrome, and Conduction Defect.
Veltmann C et al.
Journal of the American Heart Association, 2016
Transforming Growth Factor-β1 T869C Gene Polymorphism Is Associated with Acquired Sick Sinus Syndrome via Linking a Higher Serum Protein Level.
Chen JY et al.
Plos One, 2016
SCN5A mutation in Chinese patients with arrhythmogenic right ventricular dysplasia.
Yu J et al.
Herz, 2014
A novel strategy using cardiac sodium channel polymorphic fragments to rescue trafficking-deficient SCN5A mutations.
Shinlapawittayatorn K et al.
Circulation. Cardiovascular Genetics, 2011
Mutation-specific effects of polymorphism H558R in SCN5A-related sick sinus syndrome.
Gui J et al.
Journal of Cardiovascular Electrophysiology, 2010
Postmortem molecular analysis of KCNQ1 and SCN5A genes in sudden unexplained death in young Australians.
Doolan A et al.
International Journal of Cardiology, 2008
A sodium channel pore mutation causing Brugada syndrome.
Pfahnl AE et al.
Heart Rhythm, 2007
[Single nucleotide polymorphism in SCN5A and the distribution in Chinese Han ethnic group].
Xie XD et al.
Sheng Li Xue Bao : [acta Physiologica Sinica], 2004
A common SCN5A polymorphism modulates the biophysical effects of an SCN5A mutation.
Viswanathan PC et al.
The Journal of Clinical Investigation, 2003
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