Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navβ4 peptide-mediated resurgent sodium currents

Journal of Physiology

Volumn 589, Issue 3, 2011, Pages 597-608

  Theile, Jonathan W ^a   Jarecki, Brian W ^a   Piekarz, Andrew D ^a   Cummins, Theodore R ^a  

^a INDIANA UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PEPTIDE DERIVATIVE; PEPTIDE NAVBETA4; SODIUM CHANNEL NAV1.7; UNCLASSIFIED DRUG;

AMPLITUDE MODULATION; ARTICLE; CELL STRAIN HEK293; CHANNEL GATING; CONTROLLED STUDY; ERYTHROMELALGIA; HUMAN; HUMAN CELL; MISSENSE MUTATION; MUTANT; NERVE CELL EXCITABILITY; PAIN; PAROXYSMAL EXTREME PAIN DISORDER; PRIORITY JOURNAL; PROTEIN FUNCTION; REPOLARIZATION; SODIUM CURRENT; SPINAL GANGLION; WILD TYPE;

AMINO ACID SUBSTITUTION; ELECTROPHYSIOLOGICAL PHENOMENA; ERYTHROMELALGIA; HEK293 CELLS; HUMANS; ION CHANNEL GATING; MEMBRANE POTENTIALS; MUTATION, MISSENSE; NEURALGIA; PATCH-CLAMP TECHNIQUES; PEPTIDE FRAGMENTS; SODIUM CHANNELS; TRANSFECTION;

EID: 79251569257     PISSN: 00223751     EISSN: 14697793     Source Type: Journal    
DOI: 10.1113/jphysiol.2010.200915     Document Type: Article

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