Publications
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Filters: Author is Boutjdir, Mohamed [Clear All Filters]
“Ethnic and racial differences in Asian populations with ion channelopathies associated with sudden cardiac death.”, Front Cardiovasc Med, vol. 10, p. 1253479, 2023.
“Generation of four myotonic dystrophy type 1 patient iPSC lines (CBRCULi002-A, CBRCULi003-A, CBRCULi004-A, CBRCULi005-A) and a control (CBRCULi001-A) derived from lymphoblastoids cell lines.”, Stem Cell Res, vol. 67, p. 103037, 2023.
“Lymphoblastoid cell lines derived from iPSCs of a myotonic dystrophy type 1 patient carrying 700 CTG repeats (CBRCULi007-A) and a control (CBRCULi006-A).”, Stem Cell Res, vol. 71, p. 103148, 2023.
“Optical Mapping of Cardiomyocytes in Monolayer Derived from Induced Pluripotent Stem Cells.”, Cells, vol. 12, no. 17, 2023.
“Pathophysiology of Ca1.3 L-type calcium channels in the heart.”, Front Physiol, vol. 14, p. 1144069, 2023.
“Enhanced Delivery of Ligand-Conjugated Antisense Oligonucleotides (C16-HA-ASO) Targeting Dystrophia Myotonica Protein Kinase Transcripts for the Treatment of Myotonic Dystrophy Type 1.”, Hum Gene Ther, vol. 33, no. 15-16, pp. 810-820, 2022.
“Racial Disparities in Ion Channelopathies and Inherited Cardiovascular Diseases Associated With Sudden Cardiac Death.”, J Am Heart Assoc, vol. 11, no. 6, p. e023446, 2022.
“Recent Progress and Challenges in the Development of Antisense Therapies for Myotonic Dystrophy Type 1.”, Int J Mol Sci, vol. 23, no. 21, 2022.
, “Interleukin-6 inhibition of hERG underlies risk for acquired long QT in cardiac and systemic inflammation.”, PLoS One, vol. 13, no. 12, p. e0208321, 2018.
, “Biophysical, Molecular, and Pharmacological Characterization of Voltage-Dependent Sodium Channels From Induced Pluripotent Stem Cell-Derived Cardiomyocytes.”, Can J Cardiol, vol. 33, no. 2, pp. 269-278, 2017.
, “Induced pluripotent stem-cell-derived cardiomyocytes: cardiac applications, opportunities, and challenges.”, Can J Physiol Pharmacol, vol. 95, no. 10, pp. 1108-1116, 2017.
, “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, vol. 594, no. 21, pp. 6175-6187, 2016.
, “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.
, “Pathogenesis of the Novel Autoimmune-Associated Long-QT Syndrome.”, Circulation, vol. 132, no. 4, pp. 230-40, 2015.
, “Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutation.”, Front Pharmacol, vol. 4, p. 126, 2013.
, “Perinatal and postnatal expression of Cav1.3 α1D Ca²⁺ channel in the rat heart.”, Pediatr Res, vol. 69, no. 6, pp. 479-84, 2011.
, “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.
, “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.
, “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.
, “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.
, “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.
