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Mexiletine differentially restores the trafficking defects caused by two brugada syndrome mutations. Front Pharmacol. 2012;3:62.
Y1767C, a novel SCN5A mutation, induces a persistent Na+ current and potentiates ranolazine inhibition of Nav1.5 channels. Am J Physiol Heart Circ Physiol. 2011;300(1):H288-99.
Cell membrane expression of cardiac sodium channel Na(v)1.5 is modulated by alpha-actinin-2 interaction. Biochemistry. 2010;49(1):166-78.
Biophysical characterization of a new SCN5A mutation S1333Y in a SIDS infant linked to long QT syndrome. FEBS Lett. 2009;583(5):890-6.
Contribution of long-QT syndrome genetic variants in sudden infant death syndrome. Pediatr Cardiol. 2009;30(4):502-9.
Gain-of-function mutation of Nav1.5 in atrial fibrillation enhances cellular excitability and lowers the threshold for action potential firing. Biochem Biophys Res Commun. 2009;380(1):132-7.
In utero onset of long QT syndrome with atrioventricular block and spontaneous or lidocaine-induced ventricular tachycardia: compound effects of hERG pore region mutation and SCN5A N-terminus variant. Heart Rhythm. 2008;5(11):1567-74.
A novel mutation in the SCN5A gene is associated with Brugada syndrome. Life Sci. 2007;80(8):716-24.
A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation. Cardiovasc Res. 2006;70(3):521-9.