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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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Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons

The Journal of neuroscience, 2013-08, Vol.33 (35), p.14087-14097

2013

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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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Nav1.3 Sodium Channels: Rapid Repriming and Slow Closed-State Inactivation Display Quantitative Differences after Expression in a Mammalian Cell Line and in Spinal Sensory Neurons

The Journal of neuroscience, 2001-08, Vol.21 (16), p.5952-5961

2001

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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 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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The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy

Neuromolecular medicine, 2015-06, Vol.17 (2), p.158-169

2015

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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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NaN, a Novel Voltage-Gated Na Channel, is Expressed Preferentially in Peripheral Sensory Neurons and Down-Regulated after Axotomy

Proceedings of the National Academy of Sciences - PNAS, 1998-07, Vol.95 (15), p.8963-8968

1998

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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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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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Transfection of rat or mouse neurons by biolistics or electroporation

Nature protocols, 2009-08, Vol.4 (8), p.1118-1127

2009

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Antihypertensive and vasorelaxant effects of aqueous extract of Artemisia campestris L. from Eastern Morocco

Journal of ethnopharmacology, 2017-07, Vol.206, p.224-235

2017

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GDNF and NGF Reverse Changes in Repriming of TTX-Sensitive Na+ Currents Following Axotomy of Dorsal Root Ganglion Neurons

Journal of neurophysiology, 2002-08, Vol.88 (2), p.650-658

2002

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Voltage-Gated Sodium Channel Nav1.6 Is Modulated by p38 Mitogen-Activated Protein Kinase

The Journal of neuroscience, 2005-07, Vol.25 (28), p.6621-6630

2005

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Glycosylation Alters Steady-State Inactivation of Sodium Channel Nav1.9/NaN in Dorsal Root Ganglion Neurons and Is Developmentally Regulated

The Journal of neuroscience, 2001-12, Vol.21 (24), p.9629-9637

2001

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Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension

Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-13

2017

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Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons

Brain research. Molecular brain research., 1999-04, Vol.67 (2), p.267-282

1999

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Fibroblast Growth Factor Homologous Factor 1B Binds to the C Terminus of the Tetrodotoxin-resistant Sodium Channel rNav1.9a (NaN)

The Journal of biological chemistry, 2001-06, Vol.276 (22), p.18925-18933

2001

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An ankyrinG-binding motif is necessary and sufficient for targeting Nav1.6 sodium channels to axon initial segments and nodes of Ranvier

The Journal of neuroscience, 2012-05, Vol.32 (21), p.7232-7243

2012

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NGF has opposing effects on Na+ channel III and SNS gene expression in spinal sensory neurons

Neuroreport, 1997-07, Vol.8 (9), p.2331-2335

1997

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The effect of intestinal ischemia and reperfusion injury on ICAM-1 expression, endothelial barrier function, neutrophil tissue influx, and protease inhibitor levels in rats

Shock (Augusta, Ga.), 2002-07, Vol.18 (1), p.86-92

2002

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Food and water intake suppression by intracerebroventricular administration of substance P in food- and water-deprived rats

Brain research, 1999-05, Vol.830 (1), p.38-42

Dib, Bassam

1999

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Coding Sequence, Genomic Organization, and Conserved Chromosomal Localization of the Mouse Gene Scn11a Encoding the Sodium Channel NaN

Genomics (San Diego, Calif.), 1999-08, Vol.59 (3), p.309-318

1999

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Early- and late-onset inherited erythromelalgia: genotype–phenotype correlation

Brain (London, England : 1878), 2009-07, Vol.132 (7), p.1711-1722

2009

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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

Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons

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

Nav1.3 Sodium Channels: Rapid Repriming and Slow Closed-State Inactivation Display Quantitative Differences after Expression in a Mammalian Cell Line and in Spinal Sensory Neurons

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

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

The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy

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

NaN, a Novel Voltage-Gated Na Channel, is Expressed Preferentially in Peripheral Sensory Neurons and Down-Regulated after Axotomy

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

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

Transfection of rat or mouse neurons by biolistics or electroporation

Antihypertensive and vasorelaxant effects of aqueous extract of Artemisia campestris L. from Eastern Morocco

GDNF and NGF Reverse Changes in Repriming of TTX-Sensitive Na+ Currents Following Axotomy of Dorsal Root Ganglion Neurons

Voltage-Gated Sodium Channel Nav1.6 Is Modulated by p38 Mitogen-Activated Protein Kinase

Glycosylation Alters Steady-State Inactivation of Sodium Channel Nav1.9/NaN in Dorsal Root Ganglion Neurons and Is Developmentally Regulated

Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension

Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons

Fibroblast Growth Factor Homologous Factor 1B Binds to the C Terminus of the Tetrodotoxin-resistant Sodium Channel rNav1.9a (NaN)

An ankyrinG-binding motif is necessary and sufficient for targeting Nav1.6 sodium channels to axon initial segments and nodes of Ranvier

NGF has opposing effects on Na+ channel III and SNS gene expression in spinal sensory neurons

The effect of intestinal ischemia and reperfusion injury on ICAM-1 expression, endothelial barrier function, neutrophil tissue influx, and protease inhibitor levels in rats

Food and water intake suppression by intracerebroventricular administration of substance P in food- and water-deprived rats

Coding Sequence, Genomic Organization, and Conserved Chromosomal Localization of the Mouse Gene Scn11a Encoding the Sodium Channel NaN

Early- and late-onset inherited erythromelalgia: genotype–phenotype correlation

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