Mutations at opposite Ends of the DIII/S4-S5 Linker of Sodium Channel NaV1.7 Produce Distinct Pain Disorders

A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia

(2009) Tanya Z. Fischer et al.   ANNALS OF NEUROLOGY

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

(2009) Chongyang Han et al.   BRAIN

Mexiletine-responsive erythromelalgia due to a new Nav1.7 mutation showing use-dependent current fall-off

(2009) Jin-Sung Choi et al.   EXPERIMENTAL NEUROLOGY

Transfection of rat or mouse neurons by biolistics or electroporation

(2009) Sulayman D Dib-Hajj et al.   Nature Protocols

Cryptogenic Epileptic Syndromes Related to SCN1A

(2008) Claudio Zucca et al.   ARCHIVES OF NEUROLOGY

NaV1.7 Gain-of-Function Mutations as a Continuum: A1632E Displays Physiological Changes Associated with Erythromelalgia and Paroxysmal Extreme Pain Disorder Mutations and Produces Symptoms of Both Disorders

(2008) M. Estacion et al.   JOURNAL OF NEUROSCIENCE

Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation

(2008) Brian W. Jarecki et al.   JOURNAL OF PHYSIOLOGY-LONDON

Paroxysmal Extreme Pain Disorder M1627K Mutation in Human Nav1.7 Renders DRG Neurons Hyperexcitable

(2008) Sulayman D Dib-Hajj et al.   Molecular Pain

Mutation I136V Alters Electrophysiological Properties of the NaV1.7 Channel in a Family with Onset of Erythromelalgia in the Second Decade

(2008) Xiaoyang Cheng et al.   Molecular Pain