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Interleukin-6 inhibition of hERG underlies risk for acquired long QT in cardiac and systemic inflammation. PLoS ONE. 2018;13(12):e0208321.
Biophysical, Molecular, and Pharmacological Characterization of Voltage-Dependent Sodium Channels From Induced Pluripotent Stem Cell-Derived Cardiomyocytes. Can J Cardiol. 2017;33(2):269-278.
Induced pluripotent stem-cell-derived cardiomyocytes: cardiac applications, opportunities, and challenges. Can J Physiol Pharmacol. 2017;95(10):1108-1116.
Regulation of Cardiac Voltage-Gated Sodium Channel by Kinases: Roles of Protein Kinases A and C. Handb Exp Pharmacol. 2017.
Induction of autoimmune response to the extracellular loop of the HERG channel pore induces QTc prolongation in guinea-pigs. J Physiol (Lond). 2016;594(21):6175-6187.
Mutations in the Voltage Sensors of Domains I and II of Nav1.5 that are Associated with Arrhythmias and Dilated Cardiomyopathy Generate Gating Pore Currents. Front Pharmacol. 2015;6:301.
Pathogenesis of the Novel Autoimmune-Associated Long-QT Syndrome. Circulation. 2015;132(4):230-40.
Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation. Front Pharmacol. 2013;4:126.
Perinatal and postnatal expression of Cav1.3 α1D Ca²⁺ channel in the rat heart. Pediatr Res. 2011;69(6):479-84.
Phosphorylation of the consensus sites of protein kinase A on alpha1D L-type calcium channel. J Biol Chem. 2009;284(8):5042-9.
Expression of skeletal muscle Na(V)1.4 Na channel isoform in canine cardiac Purkinje myocytes. Biochem Biophys Res Commun. 2007;355(1):28-33.
Protein kinase C activation inhibits Cav1.3 calcium channel at NH2-terminal serine 81 phosphorylation site. Am J Physiol Heart Circ Physiol. 2006;291(4):H1614-22.
Modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by protein kinase A and protein kinase C. J Neurophysiol. 2004;91(4):1556-69.