Sodium channel protein type X subunit alpha (where X is the subtype, e.g., 1, 2, ... 9; must be specified for complete structure[4][6]) (NavX.X (e.g., Nav1.1 for type 1 sodium channel)[4][6])

The alpha subunit of voltage-dependent sodium channels is a large, transmembrane protein (∼260 kDa) organized into four homologous domains (I–IV), each containing six transmembrane segments (S1–S6), which together form a central pore for sodium ions[4][3][1]. The channel's opening is triggered by changes in membrane potential, allowing the influx of sodium ions and the generation of action potentials in nerves, muscles, and neuroendocrine cells[3][1]. The alpha subunit alone can form a functional channel, though auxiliary beta subunits (β1-β4) modulate its kinetics, cell surface expression, and localization[4][1]. Mutations in the alpha subunits cause a wide variety of inherited or acquired diseases (channelopathies), and the alpha subunit is the principal site of action for anti-epileptic, antiarrhythmic, local anesthetic, and analgesic drugs[5][3][4][6].

Other names

Voltage-gated sodium channel alpha subunitSodium channel alpha subunitSCNxA (where x = subtype number; e.g., SCN1A, SCN2A, etc.)Nav alpha subunit

Blockade of channel pore (inhibiting sodium influx) Stabilization of inactivated state Modulation of gating kinetics (including fast and slow inactivation)[5][4][3]