Associated Papers
Genetic and Clinical Insights into Inherited Erythromelalgia: A Comprehensive Review of Cases from China and Worldwide.
Li Y et al.
The Journal of Investigative Dermatology, 2026
Unwinding and spiral sliding of S4 and domain rotation of VSD during the electromechanical coupling in Nav1.7.
Huang G et al.
Proceedings of the National Academy of Sciences of the United States of America, 2022
Network topology of NaV1.7 mutations in sodium channel-related painful disorders.
Kapetis D et al.
Bmc Systems Biology, 2017
Nav1.7-A1632G Mutation from a Family with Inherited Erythromelalgia: Enhanced Firing of Dorsal Root Ganglia Neurons Evoked by Thermal Stimuli.
Yang Y et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2016
Short-lasting unilateral neuralgiform headache attacks with ispilateral facial flushing is a new variant of paroxysmal extreme pain disorder.
Imai N et al.
The Journal of Headache and Pain, 2015
A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers.
Wu MT et al.
Plos One, 2013
Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy.
Han C et al.
Brain : a Journal of Neurology, 2012
Severe case and literature review of primary erythromelalgia: novel SCN9A gene mutation.
Skeik N et al.
Vascular Medicine (london, England), 2012
Pain perception is altered by a nucleotide polymorphism in SCN9A.
Reimann F et al.
Proceedings of the National Academy of Sciences of the United States of America, 2010
A role of SCN9A in human epilepsies, as a cause of febrile seizures and as a potential modifier of Dravet syndrome.
Singh NA et al.
Plos Genetics, 2009
Characterization of a familial case with primary erythromelalgia from Taiwan.
Lee MJ et al.
Journal of Neurology, 2007
Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia.
Yang Y et al.
Journal of Medical Genetics, 2004
Novel SCN9A missense mutations contribute to congenital insensitivity to pain: Unexpected correlation between electrophysiological characterization and clinical phenotype.
Sun J et al.
Molecular Pain, 0
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