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No Pain, No Gain of Function: Epilepsy-Associated Variants in SCN2A Defy Classification

Epilepsy currents, 2024-04, Vol.24 (2), p.126-128

2024

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Inter-Regulation of Kv4.3 and Voltage-Gated Sodium Channels Underlies Predisposition to Cardiac and Neuronal Channelopathies

International journal of molecular sciences, 2020-07, Vol.21 (14), p.5057

2020

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Trafficking and Gating Cooperation Between Deficient Nav1.5-mutant Channels to Rescue INa

Frontiers in bioscience (Landmark. Print), 2022-06, Vol.27 (7), p.209-209

2022

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Voltage-gated sodium channels assemble and gate as dimers

Nature communications, 2017-12, Vol.8 (1), p.2077-14, Article 2077

2017

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SCN1A gain‐of‐function mutation causing an early onset epileptic encephalopathy

Epilepsia (Copenhagen), 2023-05, Vol.64 (5), p.1318-1330

2023

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Acacetin suppresses the electrocardiographic and arrhythmic manifestations of the J wave syndromes

PloS one, 2020-11, Vol.15 (11), p.e0242747

2020

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Targeted blockade of aberrant sodium current in a stem cell-derived neuron model of SCN3A encephalopathy

Brain (London, England : 1878), 2024-04, Vol.147 (4), p.1247-1263

2024

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The voltage-gated sodium channel pore exhibits conformational flexibility during slow inactivation

The Journal of general physiology, 2018-09, Vol.150 (9), p.1333-1347

2018

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Dominant-negative effect of SCN5A N-terminal mutations through the interaction of Na(v)1.5 α-subunits

Cardiovascular research, 2012-10, Vol.96 (1), p.53-63

2012

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A truncating SCN5A mutation combined with genetic variability causes sick sinus syndrome and early atrial fibrillation

Heart rhythm, 2014-06, Vol.11 (6), p.1015-1023

2014

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A KCNC1‐related neurological disorder due to gain of Kv3.1 function

Annals of clinical and translational neurology, 2023-01, Vol.10 (1), p.111-117

2023

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Mutant voltage-gated Na + channels can exert a dominant negative effect through coupled gating

American journal of physiology. Heart and circulatory physiology, 2018-11, Vol.315 (5), p.H1250-H1257

2018

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Mutations in NaV1.5 Reveal Calcium-Calmodulin Regulation of Sodium Channel

Frontiers in physiology, 2019-06, Vol.10, p.700-700

2019

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Dominant-negative effect of SCN5A N-terminal mutations through the interaction of Nav1.5 α-subunits

Cardiovascular research, 2012-10, Vol.96 (1), p.53-63

2012

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Inter-Regulation of K v 4.3 and Voltage-Gated Sodium Channels Underlies Predisposition to Cardiac and Neuronal Channelopathies

International journal of molecular sciences, 2020-07, Vol.21 (14)

2020

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Trafficking and Gating Cooperation Between Deficient Nav1.5-mutant Channels to Rescue INa

Frontiers in bioscience (Landmark. Print), 2022-06, Vol.27

2022

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Mutant voltage-gated Na^sup +^ channels can exert a dominant negative effect through coupled gating

American journal of physiology. Heart and circulatory physiology, 2018-11, Vol.315 (5), p.H1250

2018

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Mutant voltage-gated Na+ channels can exert a dominant negative effect through coupled gating

American journal of physiology. Heart and circulatory physiology, 2018-08, Vol.315 (5), p.H1250-H1257

2018

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Interaction of the Cardiac Sodium Channel Alpha-Subunits Leads to Coupled Gating Properties

Biophysical journal, 2015-01, Vol.108 (2), p.572a-572a

2015

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Mutant voltage-gated Na + channels can exert a dominant negative effect through coupled gating

American journal of physiology. Heart and circulatory physiology, 2018-11, Vol.315 (5), p.H1250

2018

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A structurally precise mechanism links an epilepsy-associated KCNC2 potassium channel mutation to interneuron dysfunction

Proceedings of the National Academy of Sciences - PNAS, 2024-01, Vol.121 (3), p.e2307776121

2024

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Distinct Features of Probands With Early Repolarization and Brugada Syndromes Carrying SCN5A Pathogenic Variants

Journal of the American College of Cardiology, 2021-10, Vol.78 (16), p.1603-1617

2021

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Voltage-Gated Sodium Channel Mutations can Exert Dominant-Negative Suppression by Coupled Gating

Biophysical journal, 2017-02, Vol.112 (3), p.104a-104a

2017

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Role of the Cytoplasmic N-Terminal Domain of the Cardiac Sodium Channel Alpha-Subunit

Biophysical journal, 2012-01, Vol.102 (3), p.527a-527a

2012

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No Pain, No Gain of Function: Epilepsy-Associated Variants in SCN2A Defy Classification

Inter-Regulation of Kv4.3 and Voltage-Gated Sodium Channels Underlies Predisposition to Cardiac and Neuronal Channelopathies

Trafficking and Gating Cooperation Between Deficient Nav1.5-mutant Channels to Rescue INa

Voltage-gated sodium channels assemble and gate as dimers

SCN1A gain‐of‐function mutation causing an early onset epileptic encephalopathy

Acacetin suppresses the electrocardiographic and arrhythmic manifestations of the J wave syndromes

Targeted blockade of aberrant sodium current in a stem cell-derived neuron model of SCN3A encephalopathy

The voltage-gated sodium channel pore exhibits conformational flexibility during slow inactivation

Dominant-negative effect of SCN5A N-terminal mutations through the interaction of Na(v)1.5 α-subunits

A truncating SCN5A mutation combined with genetic variability causes sick sinus syndrome and early atrial fibrillation

A KCNC1‐related neurological disorder due to gain of Kv3.1 function

Mutant voltage-gated Na + channels can exert a dominant negative effect through coupled gating

Mutations in NaV1.5 Reveal Calcium-Calmodulin Regulation of Sodium Channel

Dominant-negative effect of SCN5A N-terminal mutations through the interaction of Nav1.5 α-subunits

Inter-Regulation of K v 4.3 and Voltage-Gated Sodium Channels Underlies Predisposition to Cardiac and Neuronal Channelopathies

Trafficking and Gating Cooperation Between Deficient Nav1.5-mutant Channels to Rescue INa

SCN3A‐Related Neurodevelopmental Disorder: A Spectrum of Epilepsy and Brain Malformation

Mutant voltage-gated Na^sup +^ channels can exert a dominant negative effect through coupled gating

Mutant voltage-gated Na+ channels can exert a dominant negative effect through coupled gating

Interaction of the Cardiac Sodium Channel Alpha-Subunits Leads to Coupled Gating Properties

Mutant voltage-gated Na + channels can exert a dominant negative effect through coupled gating

A structurally precise mechanism links an epilepsy-associated KCNC2 potassium channel mutation to interneuron dysfunction

Distinct Features of Probands With Early Repolarization and Brugada Syndromes Carrying SCN5A Pathogenic Variants

Voltage-Gated Sodium Channel Mutations can Exert Dominant-Negative Suppression by Coupled Gating

Role of the Cytoplasmic N-Terminal Domain of the Cardiac Sodium Channel Alpha-Subunit

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