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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 Normal and Pathological Pain

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

2010

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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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A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain

Frontiers in neuroscience, 2019-09, Vol.13, p.918-918

2019

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CSF Monoamine Metabolites in Relation to the Diagnostic Interview for Borderline Patients (DIB)

Neuropsychobiology, 1998-11, Vol.38 (4), p.207-212

1998

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The Na(V)1.7 sodium channel: from molecule to man

Nature reviews. Neuroscience, 2013-01, Vol.14 (1), p.49

2013

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Sodium channels in pain disorders: pathophysiology and prospects for treatment

Pain (Amsterdam), 2017-04, Vol.158 Suppl 1, p.S97

2017

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NaV1.7: A central role in pain

Neuron (Cambridge, Mass.), 2023-09, Vol.111 (17), p.2615-2617

2023

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A Novel Persistent Tetrodotoxin-Resistant Sodium Current In SNS-Null And Wild-Type Small Primary Sensory Neurons

The Journal of neuroscience, 1999-12, Vol.19 (24), p.43-RC43

1999

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Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy

Annals of neurology, 2012-01, Vol.71 (1), p.26-39

2012

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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 sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons

Experimental neurology, 2010-08, Vol.224 (2), p.362-368

2010

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A sodium channel gene SCN9A polymorphism that increases nociceptor excitability

Annals of neurology, 2009-12, Vol.66 (6), p.862-866

2009

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Maximizing treatment efficacy through patient stratification in neuropathic pain trials

Nature reviews. Neurology, 2023-01, Vol.19 (1), p.53-64

2023

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Familial trigeminal neuralgia – a systematic clinical study with a genomic screen of the neuronal electrogenisome

Cephalalgia, 2020-07, Vol.40 (8), p.767-777

2020

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Inherited Neuronal Ion Channelopathies: New Windows on Complex Neurological Diseases

The Journal of neuroscience, 2008-11, Vol.28 (46), p.11768-11777

2008

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Physiological and genetic analysis of multiple sodium channel variants in a model of genetic absence epilepsy

Neurobiology of disease, 2014-07, Vol.67, p.180-190

2014

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Fibroblast growth factor homologous factor 2 attenuates excitability of DRG neurons

Journal of neurophysiology, 2022-11, Vol.128 (5), p.1258-1266

2022

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Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain

Pain (Amsterdam), 1999-12, Vol.83 (3), p.591-600

1999

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FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels

Molecular and cellular neuroscience, 2009-09, Vol.42 (2), p.90-101

2009

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Erythromelalgia: A hereditary pain syndrome enters the molecular era

Annals of neurology, 2005-06, Vol.57 (6), p.785-788

2005

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Mini-review - Sodium channels and beyond in peripheral nerve disease: Modulation by cytokines and their effector protein kinases

Neuroscience letters, 2021-01, Vol.741, p.135446-135446, Article 135446

2021

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KCNQ variants and pain modulation: a missense variant in Kv7.3 contributes to pain resilience

Brain communications, 2021-01, Vol.3 (3), p.fcab212-fcab212

2021

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Multistate structural modeling and voltage-clamp analysis of epilepsy/autism mutation Kv10.2-R327H demonstrate the role of this residue in stabilizing the channel closed state

The Journal of neuroscience, 2013-10, Vol.33 (42), p.16586-16593

2013

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Recent advances for using human induced-pluripotent stem cells as pain-in-a-dish models of neuropathic pain

Experimental neurology, 2022-12, Vol.358, p.114223-114223, Article 114223

2022

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

Sodium Channels in Normal and Pathological Pain

Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics

A Novel Gain-of-Function Nav1.9 Mutation in a Child With Episodic Pain

CSF Monoamine Metabolites in Relation to the Diagnostic Interview for Borderline Patients (DIB)

The Na(V)1.7 sodium channel: from molecule to man

Sodium channels in pain disorders: pathophysiology and prospects for treatment

NaV1.7: A central role in pain

A Novel Persistent Tetrodotoxin-Resistant Sodium Current In SNS-Null And Wild-Type Small Primary Sensory Neurons

Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy

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

A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons

A sodium channel gene SCN9A polymorphism that increases nociceptor excitability

Maximizing treatment efficacy through patient stratification in neuropathic pain trials

Familial trigeminal neuralgia – a systematic clinical study with a genomic screen of the neuronal electrogenisome

Inherited Neuronal Ion Channelopathies: New Windows on Complex Neurological Diseases

Physiological and genetic analysis of multiple sodium channel variants in a model of genetic absence epilepsy

Fibroblast growth factor homologous factor 2 attenuates excitability of DRG neurons

Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain

FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels

Erythromelalgia: A hereditary pain syndrome enters the molecular era

Mini-review - Sodium channels and beyond in peripheral nerve disease: Modulation by cytokines and their effector protein kinases

KCNQ variants and pain modulation: a missense variant in Kv7.3 contributes to pain resilience

Multistate structural modeling and voltage-clamp analysis of epilepsy/autism mutation Kv10.2-R327H demonstrate the role of this residue in stabilizing the channel closed state

Recent advances for using human induced-pluripotent stem cells as pain-in-a-dish models of neuropathic pain

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