Publications
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Filters: Author is Mohamed Chahine [Clear All Filters]
, “Regulation of Nav1.6 and Nav1.8 peripheral nerve Na+ channels by auxiliary β-subunits.”, J Neurophysiol, vol. 106, no. 2, pp. 608-19, 2011.
, “Regulatory Role of Voltage-Gated Na Channel β Subunits in Sensory Neurons.”, Front Pharmacol, vol. 2, p. 70, 2011.
, “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.
, “Biophysical characterisation of the persistent sodium current of the Nav1.6 neuronal sodium channel: a single-channel analysis.”, Pflugers Arch, vol. 460, no. 1, pp. 77-86, 2010.
, “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.
, “Congenital heart block: identification of autoantibody binding site on the extracellular loop (domain I, S5-S6) of alpha(1D) L-type Ca channel.”, J Autoimmun, vol. 34, no. 2, pp. 80-6, 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.
, “Cardiac metabolic state and Brugada syndrome: a link revealed.”, Circ Res, vol. 105, no. 8, pp. 721-3, 2009.
, “Characterization of novel KCNH2 mutations in type 2 long QT syndrome manifesting as seizures.”, Can J Cardiol, vol. 25, no. 8, pp. 455-62, 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.
, “Phosphorylation of the consensus sites of protein kinase A on alpha1D L-type calcium channel.”, J Biol Chem, vol. 284, no. 8, pp. 5042-9, 2009.
, “Biophysical properties of human Na v1.7 splice variants and their regulation by protein kinase A.”, J Neurophysiol, vol. 99, no. 5, pp. 2241-50, 2008.
, “Changes in action potentials and intracellular ionic homeostasis in a ventricular cell model related to a persistent sodium current in SCN5A mutations underlying LQT3.”, Prog Biophys Mol Biol, vol. 96, no. 1-3, pp. 281-93, 2008.
, “Enzyme domain affects the movement of the voltage sensor in ascidian and zebrafish voltage-sensing phosphatases.”, J Biol Chem, vol. 283, no. 26, pp. 18248-59, 2008.
, “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 new C-terminal hERG mutation A915fs+47X associated with symptomatic LQT2 and auditory-trigger syncope.”, Heart Rhythm, vol. 5, no. 11, pp. 1577-86, 2008.
, “The occurrence of Brugada syndrome and isolated cardiac conductive disease in the same family could be due to a single SCN5A mutation or to the accidental association of both diseases.”, Europace, vol. 10, no. 1, pp. 79-85, 2008.
, “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.
