Mohamed Yassine Amarouch
Affiliations: | 2011-2014 | University of Bern, Bern, Bern, Switzerland |
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Publications
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| Amarouch MY, El Hilaly J. (2020) Inherited Cardiac Arrhythmia Syndromes: Focus on Molecular Mechanisms Underlying TRPM4 Channelopathies. Cardiovascular Therapeutics. 2020: 6615038 |
| Amarouch MY, Kurt H, Delemotte L, et al. (2020) Biophysical Characterization of Epigallocatechin-3-Gallate Effect on the Cardiac Sodium Channel Na1.5. Molecules (Basel, Switzerland). 25 |
| Boukhabza M, El Hilaly J, Attiya N, et al. (2016) Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies. Computational and Mathematical Methods in Medicine. 2016: 7861653 |
| Syam N, Chatel S, Ozhathil LC, et al. (2016) Variants of Transient Receptor Potential Melastatin Member 4 in Childhood Atrioventricular Block. Journal of the American Heart Association. 5 |
| Amarouch MY, Swan H, Leinonen J, et al. (2016) Antiarrhythmic Action of Flecainide in Polymorphic Ventricular Arrhythmias Caused by a Gain-of-Function Mutation in the Nav 1.5 Sodium Channel. Annals of Noninvasive Electrocardiology : the Official Journal of the International Society For Holter and Noninvasive Electrocardiology, Inc. 21: 343-51 |
| Daumy X, Amarouch MY, Lindenbaum P, et al. (2016) Targeted resequencing identifies TRPM4 as a major gene predisposing to progressive familial heart block type I. International Journal of Cardiology. 207: 349-58 |
| Daumy X, Amarouch MY, Lindenbaum P, et al. (2016) Targeted resequencing identifies TRPM4 as a major gene predisposing to progressive familial heart block type i International Journal of Cardiology. 207: 349-358 |
| Amarouch MY, Abriel H. (2015) Cellular hyper-excitability caused by mutations that alter the activation process of voltage-gated sodium channels. Frontiers in Physiology. 6: 45 |
| Ossola D, Amarouch MY, Behr P, et al. (2015) Force-controlled patch clamp of beating cardiac cells. Nano Letters. 15: 1743-50 |
| Saber S, Amarouch MY, Fazelifar AF, et al. (2015) Complex genetic background in a large family with Brugada syndrome. Physiological Reports. 3 |