Publications
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“A leaky voltage sensor domain of cardiac sodium channels causes arrhythmias associated with dilated cardiomyopathy.”, Sci Rep, vol. 8, no. 1, p. 13804, 2018.
, “Biophysical, Molecular, and Pharmacological Characterization of Voltage-Dependent Sodium Channels From Induced Pluripotent Stem Cell-Derived Cardiomyocytes.”, Can J Cardiol, vol. 33, no. 2, pp. 269-278, 2017.
, “Unmasked Brugada pattern by ajmaline challenge in patients with myotonic dystrophy type 1.”, Ann Noninvasive Electrocardiol, vol. 20, no. 1, pp. 28-36, 2015.
, “Myotonic dystrophy type 1 mimics and exacerbates Brugada phenotype induced by Nav1.5 sodium channel loss-of-function mutation.”, Heart Rhythm, vol. 11, no. 8, pp. 1393-400, 2014.
, “A distinct de novo expression of Nav1.5 sodium channels in human atrial fibroblasts differentiated into myofibroblasts.”, J Physiol, vol. 590, no. 17, pp. 4307-19, 2012.
, “The β1-subunit of Na(v)1.5 cardiac sodium channel is required for a dominant negative effect through α-α interaction.”, PLoS One, vol. 7, no. 11, p. e48690, 2012.
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