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Sodium channel protein type 4 subunit alpha is the pore-forming alpha subunit of the Nav1.4 voltage-gated sodium channel. It is responsible for mediating the depolarizing phase of action potentials in excitable membranes such as skeletal muscle cells, controlling the flow of sodium ions (Na+) into muscle cells during electrical signaling required for muscle contraction and relaxation. Mutations in SCN4A have been linked to several neuromuscular disorders.
Voltage-gated sodium channels like Nav1.4 open upon membrane depolarization allowing rapid influx of Na+, which triggers further depolarization necessary for action potential propagation along nerves and muscles. Mutations alter gating properties—either causing persistent inward currents (myotonia) or inability to repolarize (paralysis)
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