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NaV1.5 knockout in iPSCs: a novel approach to study NaV1.5 variants in a human cardiomyocyte environment

Scientific reports, 2021-08, Vol.11 (1), p.17168-17168, Article 17168

2021

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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)

Stem cell research, 2024-03, Vol.75, p.103308-103308, Article 103308

2024

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De novo Y1460C missense variant in NaV1.1 impedes the pore region and results in epileptic encephalopathy

Scientific reports, 2022-10, Vol.12 (1), p.17182-17182, Article 17182

2022

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iPSC-derived cardiomyocytes from patients with myotonic dystrophy type 1 have abnormal ion channel functions and slower conduction velocities

Scientific reports, 2021-01, Vol.11 (1), p.2500-13, Article 2500

2021

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Differential modulation of Nav1.7 and Nav1.8 channels by antidepressant drugs

European journal of pharmacology, 2015-10, Vol.764, p.395-403

2015

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

The Journal of physiology, 2021-03, Vol.599 (5), p.1651-1664

2021

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R1617Q epilepsy mutation slows Na V 1.6 sodium channel inactivation and increases the persistent current and neuronal firing

The Journal of physiology, 2021-03, Vol.599 (5), p.1651-1664

2021

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Pyridoxal-5'-phosphate (MC-1), a vitamin B6 derivative, inhibits expressed P2X receptors

Canadian journal of physiology and pharmacology, 2014-03, Vol.92 (3), p.189

2014

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Nav1.5 knockout in iPSCs: a novel approach to study Nav1.5 variants in a human cardiomyocyte environment

Biophysical journal, 2022-02, Vol.121 (3), p.94a-94a

2022

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R1617Q epilepsy mutation slows NaV 1.6 sodium channel inactivation and increases the persistent current and neuronal firing

The Journal of physiology, 2021-03, Vol.599 (5), p.1651-1664

2021

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Differentiation of lymphoblastoid-derived iPSCs into functional cardiomyocytes, neurons and myoblasts

Biochemical and biophysical research communications, 2019-08, Vol.516 (1), p.222-228

2019

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Biophysical characterization of SCN1A and SCN2A variants related to epilepsy

Biophysical journal, 2022-02, Vol.121 (3), p.96a-96a

2022

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Serum- and glucocorticoid-regulated kinase 1 (SGK1) induction by the EWS/NOR1(NR4A3) fusion protein

Biochemical and biophysical research communications, 2006-07, Vol.346 (1), p.306-313

2006

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

Journal of neurophysiology, 2022-05, Vol.127 (5), p.1388-1397

2022

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A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis

Neurology, 2016-01, Vol.86 (2), p.161

2016

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Fluoxetine blocks Nav1.5 channels via a mechanism similar to that of class 1 antiarrhythmics

Molecular pharmacology, 2014-10, Vol.86 (4), p.378-389

2014

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Substitutions of the S4DIV R2 residue (R1451) in NaV1.4 lead to complex forms of paramyotonia congenita and periodic paralyses

Scientific reports, 2018-02, Vol.8 (1), p.1-13, Article 2041

2018

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Fluoxetine Blocks NaV1.5 Channels via a Mechanism Similar to that of Class 1 Antiarrhythmics

Biophysical journal, 2014-01, Vol.106 (2), p.325a-326a

2014

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De novo Y1460C missense variant in Na V 1.1 impedes the pore region and results in epileptic encephalopathy

Scientific reports, 2022-10, Vol.12 (1), p.17182

2022

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Development and Characterisation of Cardiomyocytes Derived from Murine Embryonic Stem Cells of a DCM Caused by a SCN5A Mutation

Biophysical journal, 2013-01, Vol.104 (2), p.14a-15a

2013

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Biophysical Characterization of Two Nav1.4 Mutations Identified in Patients with Cold-Induced Myotonia and Periodic Paralysis

Biophysical journal, 2016-02, Vol.110 (3), p.438a-438a

2016

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Fluoxetine Blocks Na v 1.5 Channels via a Mechanism Similar to That of Class 1 Antiarrhythmics

Molecular pharmacology, 2014-10, Vol.86 (4), p.378-389

2014

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Modulation of peripheral Na super(+) channels and neuronal firing by n-butyl-p-aminobenzoate

European journal of pharmacology, 2014-03, Vol.727, p.158-166

2014

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Autosomal Recessive Inheritance of Congenital Myasthenic Syndrome is Associated with Skeletal Muscle Sodium Channel Mutations

Biophysical journal, 2015-01, Vol.108 (2), p.491a-491a

2015

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The variant hERG/R148W associated with LQTS is a mutation that reduces current density on co-expression with the WT

Gene, 2014-02, Vol.536 (2), p.348-356

2014

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NaV1.5 knockout in iPSCs: a novel approach to study NaV1.5 variants in a human cardiomyocyte environment

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)

De novo Y1460C missense variant in NaV1.1 impedes the pore region and results in epileptic encephalopathy

iPSC-derived cardiomyocytes from patients with myotonic dystrophy type 1 have abnormal ion channel functions and slower conduction velocities

Differential modulation of Nav1.7 and Nav1.8 channels by antidepressant drugs

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

R1617Q epilepsy mutation slows Na V 1.6 sodium channel inactivation and increases the persistent current and neuronal firing

Pyridoxal-5'-phosphate (MC-1), a vitamin B6 derivative, inhibits expressed P2X receptors

Nav1.5 knockout in iPSCs: a novel approach to study Nav1.5 variants in a human cardiomyocyte environment

R1617Q epilepsy mutation slows NaV 1.6 sodium channel inactivation and increases the persistent current and neuronal firing

Differentiation of lymphoblastoid-derived iPSCs into functional cardiomyocytes, neurons and myoblasts

Biophysical characterization of SCN1A and SCN2A variants related to epilepsy

Serum- and glucocorticoid-regulated kinase 1 (SGK1) induction by the EWS/NOR1(NR4A3) fusion protein

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

A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis

Fluoxetine blocks Nav1.5 channels via a mechanism similar to that of class 1 antiarrhythmics

Substitutions of the S4DIV R2 residue (R1451) in NaV1.4 lead to complex forms of paramyotonia congenita and periodic paralyses

Fluoxetine Blocks NaV1.5 Channels via a Mechanism Similar to that of Class 1 Antiarrhythmics

De novo Y1460C missense variant in Na V 1.1 impedes the pore region and results in epileptic encephalopathy

Development and Characterisation of Cardiomyocytes Derived from Murine Embryonic Stem Cells of a DCM Caused by a SCN5A Mutation

Biophysical Characterization of Two Nav1.4 Mutations Identified in Patients with Cold-Induced Myotonia and Periodic Paralysis

Fluoxetine Blocks Na v 1.5 Channels via a Mechanism Similar to That of Class 1 Antiarrhythmics

Modulation of peripheral Na super(+) channels and neuronal firing by n-butyl-p-aminobenzoate

Autosomal Recessive Inheritance of Congenital Myasthenic Syndrome is Associated with Skeletal Muscle Sodium Channel Mutations

The variant hERG/R148W associated with LQTS is a mutation that reduces current density on co-expression with the WT

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