Publications
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, “Mexiletine differentially restores the trafficking defects caused by two brugada syndrome mutations.”, Front Pharmacol, vol. 3, p. 62, 2012.
, “A proton leak current through the cardiac sodium channel is linked to mixed arrhythmia and the dilated cardiomyopathy phenotype.”, PLoS One, vol. 7, no. 5, p. e38331, 2012.
, “Y1767C, a novel SCN5A mutation, induces a persistent Na+ current and potentiates ranolazine inhibition of Nav1.5 channels.”, Am J Physiol Heart Circ Physiol, vol. 300, no. 1, pp. H288-99, 2011.
, “Cell membrane expression of cardiac sodium channel Na(v)1.5 is modulated by alpha-actinin-2 interaction.”, Biochemistry, vol. 49, no. 1, pp. 166-78, 2010.
, “Biophysical characterization of a new SCN5A mutation S1333Y in a SIDS infant linked to long QT syndrome.”, FEBS Lett, vol. 583, no. 5, pp. 890-6, 2009.
, “Contribution of long-QT syndrome genetic variants in sudden infant death syndrome.”, Pediatr Cardiol, vol. 30, no. 4, pp. 502-9, 2009.
, “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, vol. 380, no. 1, pp. 132-7, 2009.
, “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, vol. 5, no. 11, pp. 1567-74, 2008.
, “A novel mutation in the SCN5A gene is associated with Brugada syndrome.”, Life Sci, vol. 80, no. 8, pp. 716-24, 2007.
, “A novel SCN5A mutation, F1344S, identified in a patient with Brugada syndrome and fever-induced ventricular fibrillation.”, Cardiovasc Res, vol. 70, no. 3, pp. 521-9, 2006.
