Structural Modeling of NaV-Ligand Interactions with Rosetta’s Galiganddock

Abstract

Voltage-gated sodium (NaV) channels regulate the permeation of sodium ions across voltage-dependent cell membranes, initiating action potentials in muscle and neuronal cell types. Mutations in NaV channels result in channelopathies such as pain hypersensitivity, epilepsy, migraine, and muscle paralysis. High-resolution structures of small molecules in complex with NaV channels have allowed computational biologists to study molecular mechanisms of channel gating and identify potential drug candidates to treat channelopathies.