Publications
Export 158 results:
Filtres: Author is Mohamed Chahine [Enlever les filtres]
, « Regulation of Nav1.6 and Nav1.8 peripheral nerve Na+ channels by auxiliary β-subunits. », J Neurophysiol, vol. 106, nᵒ 2, p. 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, p. 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, p. 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, p. 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, p. 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, p. 890-6, 2009.
, « Cardiac metabolic state and Brugada syndrome: a link revealed. », Circ Res, vol. 105, nᵒ 8, p. 721-3, 2009.
, « Characterization of novel KCNH2 mutations in type 2 long QT syndrome manifesting as seizures. », Can J Cardiol, vol. 25, nᵒ 8, p. 455-62, 2009.
, « Contribution of long-QT syndrome genetic variants in sudden infant death syndrome. », Pediatr Cardiol, vol. 30, nᵒ 4, p. 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, p. 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, p. 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, p. 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, p. 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, p. 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, p. 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, p. 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, p. 79-85, 2008.
, « Protein kinase C activation inhibits alpha1D L-type Ca channel: a single-channel analysis. », Pflugers Arch, vol. 455, nᵒ 5, p. 913-9, 2008.
, « Voltage-gated sodium channels in neurological disorders. », CNS Neurol Disord Drug Targets, vol. 7, nᵒ 2, p. 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, p. 169-80, 2007.
, « Acidic residues on the voltage-sensor domain determine the activation of the NaChBac sodium channel. », Biophys J, vol. 92, nᵒ 10, p. 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, p. 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, p. 467-77, 2007.
