Associated Papers
A novel SCN3B in-frame codon deletion in a Brugada syndrome patient: Implications for disrupted NaV1.5 function.
Sarbjit-Singh SS et al.
Journal of Molecular and Cellular Cardiology, 2025
Comprehensive pathological and genetic investigation of three young adult myotonic dystrophy type 1 patients with sudden unexpected death.
Hata Y et al.
Journal of Neurology, 2023
Two Novel Functional Mutations in Promoter Region of SCN3B Gene Associated with Atrial Fibrillation.
Lin L et al.
Life (basel, Switzerland), 2022
Mutations of Voltage-Gated Ionic Channels and Risk of Severe Cardiac Arrhythmias.
Dehghani-Samani A et al.
Acta Cardiologica Sinica, 2019
Cardiac channelopathies: The role of sodium channel mutations.
Fonseca DJ et al.
Revista Portuguesa De Cardiologia, 2018
Sodium channel β subunits: emerging targets in channelopathies.
O'Malley HA et al.
Annual Review of Physiology, 2015
Channelopathies from mutations in the cardiac sodium channel protein complex.
Adsit GS et al.
Journal of Molecular and Cellular Cardiology, 2013
Novel SCN3B mutation associated with brugada syndrome affects intracellular trafficking and function of Nav1.5.
Ishikawa T et al.
Circulation Journal : Official Journal of the Japanese Circulation Society, 2013
Biology of cardiac sodium channel Nav1.5 expression.
Rook MB et al.
Cardiovascular Research, 2012
Phenotypical manifestations of mutations in the genes encoding subunits of the cardiac sodium channel.
Wilde AA et al.
Circulation Research, 2011
Functional dominant-negative mutation of sodium channel subunit gene SCN3B associated with atrial fibrillation in a Chinese GeneID population.
Wang P et al.
Biochemical and Biophysical Research Communications, 2010
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