Mohamed Chahine

Laval University

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Human iPSC-derived neurons as a model of congenital myotonic dystrophy type 1

Open Date: 2021-05-03

Close Date: 2023-04-30

Articles (16)

Collaborators (2)

Christophe Proulx

Laval University

Juan Pablo Appendino

Clinical Associate Professor

University of Calgary

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Mohamed Chahine

Research Interests

Explore related searches

Contact this professor

Recent Grants

Articles (16)

Collaborators (2)

Christophe Proulx

Juan Pablo Appendino

Make your next move.

Mohamed Chahine

Research Interests

Explore related searches

Contact this professor

Recent Grants

Articles (16)

Exploring SCN5A Variants Associated with Atrial Fibrillation in Atrial Cardiomyocytes Derived from hiPSCs: A Characterization Study

Impacts of DCM-linked gating pore currents on the electrophysiological characteristics of hiPSC-CM monolayers

Arrhythmias and ion channelopathies causing sudden cardiac death in Hispanic/Latino and Indigenous populations

Generation of a lymphoblastoid-derived induced pluripotent stem cell line (CBRCULi015-A) from a patient with congenital myotonic dystrophy

Generation of a patient-specific iPSC cell line with cardiac arrhythmias and dilated cardiomyopathy (CBRCULi016-A), an isogenic control (CBRCULi016-A-1), and a paternal control (CBRCULi017-A)

Lymphoblastoid cell lines derived from iPSCs of a myotonic dystrophy type 1 patient carrying 700 CTG repeats (CBRCULi007-A) and a control (CBRCULi006-A)

Optical Mapping of Cardiomyocytes in Monolayer Derived from Induced Pluripotent Stem Cells

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

Generation of induced pluripotent stem cell lines from pediatric patients with congenital myotonic dystrophy (CBRCULi012-A and CBRCULi013-A) and age-matched controls (CBRCULi010-A and CBRCULi011-A)

SCN2A-related epilepsy of infancy with migrating focal seizures: report of a variant with apparent gain- and loss-of-function effects

NPRL2 Inhibition of mTORC1 Controls Sodium Channel Expression and Brain Amino Acid Homeostasis

Antisense oligonucleotides as a potential treatment for brain deficits observed in myotonic dystrophy type 1

Recent Progress and Challenges in the Development of Antisense Therapies for Myotonic Dystrophy Type 1

Enhanced Delivery of Ligand-Conjugated Antisense Oligonucleotides (C16-HA-ASO) Targeting Dystrophia Myotonica Protein Kinase Transcripts for the Treatment of Myotonic Dystrophy Type 1

Racial Disparities in Ion Channelopathies and Inherited Cardiovascular Diseases Associated With Sudden Cardiac Death

R1617Q epilepsy mutation slows NaV1.6 sodium channel inactivation and increases the persistent current and neuronal firing

Collaborators (2)

Christophe Proulx

Juan Pablo Appendino

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