Article

Uncoupling sodium channel dimers rescues phenotype of pain-linked Nav1.7 mutation

2019-07-27

Abstract excerpt

The voltage-gated sodium channel Nav1.7 is essential for an adequate perception of painful stimuli. Its mutations cause various pain syndromes in human patients. The hNav1.7/A1632E mutation induces symptoms of erythromelalgia and paroxysmal extreme pain disorder (PEPD), and its main gating change is a strongly enhanced persistent current. Using molecular simulations, we demonstrate that the disease causing persist...

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Literature Corpus work: e83bbdcc-7b24-5cc9-ac50-fbe1d3e162e8
DOI: 10.1101/716654

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