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Uncoupling sodium channel dimers rescues phenotype of pain-linked Nav1.7 mutation
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 persistent current of hNav1.7/A1632E is due to impaired binding of the IFM motif, thusdoi:10.1101/716654 fatcat:odcktbtsiveldnajhdr6c4j6la