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De Novo Pathogenic SCN8A Mutation Identified by Whole-Genome Sequencing of a Family Quartet Affected by Infantile Epileptic Encephalopathy and SUDEP

American journal of human genetics, 2012-03, Vol.90 (3), p.502-510

2012

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Expression of Nav1.7 in DRG Neurons Extends from Peripheral Terminals in the Skin to Central Preterminal Branches and Terminals in the Dorsal Horn

Molecular pain, 2012-11, Vol.8 (1), p.82-82

2012

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The Role of Voltage-Gated Sodium Channels in Pain Signaling

Physiological reviews, 2019-04, Vol.99 (2), p.1079-1151

2019

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Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones

The Journal of physiology, 2005-05, Vol.564 (3), p.803-815

2005

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Genetic, electrophysiological, and pathological studies on patients with SCN9A‐related pain disorders

Journal of the peripheral nervous system, 2023-12, Vol.28 (4), p.597-607

2023

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Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics

Annual review of neuroscience, 2019-07, Vol.42, p.87

2019

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Sodium Channels in Normal and Pathological Pain

Annual review of neuroscience, 2010-01, Vol.33 (1), p.325-347

2010

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Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp

The Journal of neuroscience, 2019-01, Vol.39 (3), p.382-392

2019

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Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain

Scientific reports, 2018-03, Vol.8 (1), p.1-17, Article 3845

2018

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A gain-of-function mutation in Nav1.6 in a case of trigeminal neuralgia

Molecular medicine (Cambridge, Mass.), 2016, Vol.22 (1), p.338-348

2016

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Gain-of-function Naᵥ1.8 mutations in painful neuropathy

Proceedings of the National Academy of Sciences - PNAS, 2012-11, Vol.109 (47), p.19444-19449

2012

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Gain-of-function mutations in sodium channel Nav1.9 in painful neuropathy

Brain (London, England : 1878), 2014-06, Vol.137 (6), p.1627-1642

2014

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Sodium channel genes in pain-related disorders: phenotype–genotype associations and recommendations for clinical use

Lancet neurology, 2014-11, Vol.13 (11), p.1152-1160

2014

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A TRPM7 mutation linked to familial trigeminal neuralgia: Omega current and hyperexcitability of trigeminal ganglion neurons

Proceedings of the National Academy of Sciences - PNAS, 2022-09, Vol.119 (38), p.e2119630119-e2119630119

2022

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Reverse pharmacogenomics: carbamazepine normalizes activation and attenuates thermal hyperexcitability of sensory neurons due to Na v 1.7 mutation I234T

British journal of pharmacology, 2018-06, Vol.175 (12), p.2261-2271

2018

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Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models

Pain (Amsterdam), 2020-04, Vol.161 (4), p.831-841

2020

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A novel de novo mutation of SCN8A (Nav 1.6) with enhanced channel activation in a child with epileptic encephalopathy

Neurobiology of disease, 2014-09, Vol.69, p.117-123

2014

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Voltage‐Gated Sodium Channels: Therapeutic Targets for Pain

Pain medicine (Malden, Mass.), 2009-10, Vol.10 (7), p.1260-1269

2009

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Nav1.7 is the Predominant Sodium Channel in Rodent Olfactory Sensory Neurons

Molecular pain, 2011-05, Vol.7 (1), p.32-32

2011

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Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development

PloS one, 2015-04, Vol.10 (4), p.e0124397-e0124397

2015

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Screening fluorescent voltage indicators with spontaneously spiking HEK cells

PloS one, 2013-12, Vol.8 (12), p.e85221

2013

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NaV1.6 regulates excitability of mechanosensitive sensory neurons

The Journal of physiology, 2019-07, Vol.597 (14), p.3751-3768

2019

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Chapter 4 Genetics and Molecular Pathophysiology of Nav1.7‐Related Pain Syndromes

Advanced drug delivery reviews, 2008, Vol.63, p.85-110

2008

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Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α

Cell reports (Cambridge), 2024-02, Vol.43 (2), p.113685-113685, Article 113685

2024

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A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons

Proceedings of the National Academy of Sciences - PNAS, 2006-05, Vol.103 (21), p.8245-8250

2006

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De Novo Pathogenic SCN8A Mutation Identified by Whole-Genome Sequencing of a Family Quartet Affected by Infantile Epileptic Encephalopathy and SUDEP

Expression of Nav1.7 in DRG Neurons Extends from Peripheral Terminals in the Skin to Central Preterminal Branches and Terminals in the Dorsal Horn

The Role of Voltage-Gated Sodium Channels in Pain Signaling

Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones

Genetic, electrophysiological, and pathological studies on patients with SCN9A‐related pain disorders

Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics

Sodium Channels in Normal and Pathological Pain

Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp

Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain

A gain-of-function mutation in Nav1.6 in a case of trigeminal neuralgia

Gain-of-function Naᵥ1.8 mutations in painful neuropathy

Gain-of-function mutations in sodium channel Nav1.9 in painful neuropathy

Sodium channel genes in pain-related disorders: phenotype–genotype associations and recommendations for clinical use

A TRPM7 mutation linked to familial trigeminal neuralgia: Omega current and hyperexcitability of trigeminal ganglion neurons

Reverse pharmacogenomics: carbamazepine normalizes activation and attenuates thermal hyperexcitability of sensory neurons due to Na v 1.7 mutation I234T

Dexpramipexole blocks Nav1.8 sodium channels and provides analgesia in multiple nociceptive and neuropathic pain models

A novel de novo mutation of SCN8A (Nav 1.6) with enhanced channel activation in a child with epileptic encephalopathy

Voltage‐Gated Sodium Channels: Therapeutic Targets for Pain

Nav1.7 is the Predominant Sodium Channel in Rodent Olfactory Sensory Neurons

Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development

Screening fluorescent voltage indicators with spontaneously spiking HEK cells

NaV1.6 regulates excitability of mechanosensitive sensory neurons

Chapter 4 Genetics and Molecular Pathophysiology of Nav1.7‐Related Pain Syndromes

Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α

A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons

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