Publications
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, “Protein kinase C activation inhibits alpha1D L-type Ca channel: a single-channel analysis.”, Pflugers Arch, vol. 455, no. 5, pp. 913-9, 2008.
, “Voltage-gated sodium channels in neurological disorders.”, CNS Neurol Disord Drug Targets, vol. 7, no. 2, pp. 144-58, 2008.
, “Accessibility of four arginine residues on the S4 segment of the Bacillus halodurans sodium channel.”, J Membr Biol, vol. 215, no. 2-3, pp. 169-80, 2007.
, “Acidic residues on the voltage-sensor domain determine the activation of the NaChBac sodium channel.”, Biophys J, vol. 92, no. 10, pp. 3513-23, 2007.
, “The Brugada syndrome in Canada: a unique French-Canadian experience.”, Can J Cardiol, vol. 23 Suppl B, p. 71B-75B, 2007.
, “Expression of skeletal muscle Na(V)1.4 Na channel isoform in canine cardiac Purkinje myocytes.”, Biochem Biophys Res Commun, vol. 355, no. 1, pp. 28-33, 2007.
, “Lidocaine promotes the trafficking and functional expression of Na(v)1.8 sodium channels in mammalian cells.”, J Neurophysiol, vol. 98, no. 1, pp. 467-77, 2007.
, “A novel mutation in the SCN5A gene is associated with Brugada syndrome.”, Life Sci, vol. 80, no. 8, pp. 716-24, 2007.
, “[A channel without pore? The primary structure of a proton permeable channel is finally revealed].”, Med Sci (Paris), vol. 22, no. 11, pp. 930-1, 2006.
, “Clinical aspects and physiopathology of Brugada syndrome: review of current concepts.”, Can J Physiol Pharmacol, vol. 84, no. 8-9, pp. 795-802, 2006.
, “Nav1.5/R1193Q polymorphism is associated with both long QT and Brugada syndromes.”, Can J Cardiol, vol. 22, no. 4, pp. 309-13, 2006.
, “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.
, “Protein kinase C activation inhibits Cav1.3 calcium channel at NH2-terminal serine 81 phosphorylation site.”, Am J Physiol Heart Circ Physiol, vol. 291, no. 4, pp. H1614-22, 2006.
, “SCN5A polymorphism restores trafficking of a Brugada syndrome mutation on a separate gene.”, Circulation, vol. 114, no. 5, pp. 368-76, 2006.
, “A novel nonsense mutation in the SCN5A gene leads to Brugada syndrome and a silent gene mutation carrier state.”, Can J Cardiol, vol. 21, no. 11, pp. 925-31, 2005.
, “Regulation of Na v channels in sensory neurons.”, Trends Pharmacol Sci, vol. 26, no. 10, pp. 496-502, 2005.
, “The C-terminal region as a modulator of rNa(v)1.7 and rNa(v)1.8 expression levels.”, FEBS Lett, vol. 559, no. 1-3, pp. 39-44, 2004.
, “Differential modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by the local anesthetic lidocaine.”, Br J Pharmacol, vol. 142, no. 3, pp. 576-84, 2004.
, “Genetic analysis of the cardiac sodium channel gene SCN5A in Koreans with Brugada syndrome.”, J Hum Genet, vol. 49, no. 10, pp. 573-8, 2004.
, “Loss of function associated with novel mutations of the SCN5A gene in patients with Brugada syndrome.”, Can J Cardiol, vol. 20, no. 4, pp. 425-30, 2004.
, “Modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by protein kinase A and protein kinase C.”, J Neurophysiol, vol. 91, no. 4, pp. 1556-69, 2004.
, “A novel SCN5A mutation manifests as a malignant form of long QT syndrome with perinatal onset of tachycardia/bradycardia.”, Cardiovasc Res, vol. 64, no. 2, pp. 268-78, 2004.
, “Role of arginine residues on the S4 segment of the Bacillus halodurans Na+ channel in voltage-sensing.”, J Membr Biol, vol. 201, no. 1, pp. 9-24, 2004.
, “Role of auxiliary beta1-, beta2-, and beta3-subunits and their interaction with Na(v)1.8 voltage-gated sodium channel.”, Biochem Biophys Res Commun, vol. 319, no. 2, pp. 531-40, 2004.
, “Biophysical characteristics of a new mutation on the KCNQ1 potassium channel (L251P) causing long QT syndrome.”, Can J Physiol Pharmacol, vol. 81, no. 2, pp. 129-34, 2003.
