Publications
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Filters: Author is Mohamed Chahine [Clear All Filters]
, “Molecular characterization and functional expression of the Apis mellifera voltage-dependent Ca2+ channels.”, Insect Biochem Mol Biol, vol. 58, pp. 12-27, 2015.
, “MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels.”, Front Pharmacol, vol. 6, p. 118, 2015.
, “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, vol. 6, p. 301, 2015.
, “[Omega pore, an alternative ion channel permeation pathway involved in the development of several channelopathies].”, Med Sci (Paris), vol. 31, no. 8-9, pp. 735-41, 2015.
, “Pathogenesis of the Novel Autoimmune-Associated Long-QT Syndrome.”, Circulation, vol. 132, no. 4, pp. 230-40, 2015.
, “Unmasked Brugada pattern by ajmaline challenge in patients with myotonic dystrophy type 1.”, Ann Noninvasive Electrocardiol, vol. 20, no. 1, pp. 28-36, 2015.
, “Biophysics, pathophysiology, and pharmacology of ion channel gating pores.”, Front Pharmacol, vol. 5, p. 53, 2014.
, “Correlation of the electrophysiological profiles and sodium channel transcripts of individual rat dorsal root ganglia neurons.”, Front Cell Neurosci, vol. 8, p. 285, 2014.
, “Fluoxetine blocks Nav1.5 channels via a mechanism similar to that of class 1 antiarrhythmics.”, Mol Pharmacol, vol. 86, no. 4, pp. 378-89, 2014.
, “Modulation of peripheral Na(+) channels and neuronal firing by n-butyl-p-aminobenzoate.”, Eur J Pharmacol, vol. 727, pp. 158-66, 2014.
, “Molecular biology and biophysical properties of ion channel gating pores.”, Q Rev Biophys, vol. 47, no. 4, pp. 364-88, 2014.
, “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.
, “Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?”, Channels (Austin), vol. 8, no. 1, pp. 90-4, 2014.
, “Pyrethroids differentially alter voltage-gated sodium channels from the honeybee central olfactory neurons.”, PLoS One, vol. 9, no. 11, p. e112194, 2014.
, “Pyridoxal-5'-phosphate (MC-1), a vitamin B6 derivative, inhibits expressed P2X receptors.”, Can J Physiol Pharmacol, vol. 92, no. 3, pp. 189-96, 2014.
, “Regulation/modulation of sensory neuron sodium channels.”, Handb Exp Pharmacol, vol. 221, pp. 111-35, 2014.
, “The variant hERG/R148W associated with LQTS is a mutation that reduces current density on co-expression with the WT.”, Gene, vol. 536, no. 2, pp. 348-56, 2014.
, “Characterization of the first honeybee Ca²⁺ channel subunit reveals two novel species- and splicing-specific modes of regulation of channel inactivation.”, Pflugers Arch, vol. 465, no. 7, pp. 985-96, 2013.
, “Novel SCN5A mutations in two families with "Brugada-like" ST elevation in the inferior leads and conduction disturbances.”, J Interv Card Electrophysiol, vol. 37, no. 2, pp. 131-40, 2013.
, “Recent advances in voltage-gated sodium channels, their pharmacology, and related diseases.”, Front Pharmacol, vol. 4, p. 52, 2013.
, “Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation.”, Front Pharmacol, vol. 4, p. 126, 2013.
, “Biophysical characterization of M1476I, a sodium channel founder mutation associated with cold-induced myotonia in French Canadians.”, J Physiol, vol. 590, no. 11, pp. 2629-44, 2012.
, “Coexisting mutations/polymorphisms of the long QT syndrome genes in patients with repaired Tetralogy of Fallot are associated with the risks of life-threatening events.”, Hum Genet, vol. 131, no. 8, pp. 1295-304, 2012.
, “Differential expression of sodium channel β subunits in dorsal root ganglion sensory neurons.”, J Biol Chem, vol. 287, no. 18, pp. 15044-53, 2012.
, “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.
