Sodium channel protein type 1 subunit alpha (for Nav1.1); analogous canonical forms exist for other subtypes (e.g., Nav1.2, Nav1.3, etc.) (Nav1.1 (for type 1), with other Nav subtypes (Nav1.2, Nav1.3, ... Nav1.9))

Voltage-gated sodium channel alpha subunits are the principal pore-forming components of sodium channels, which mediate rapid sodium ion influx in response to membrane depolarization in excitable cells such as neurons and cardiomyocytes. Each alpha subunit consists of four homologous transmembrane domains, each containing six transmembrane segments. The S4 segments serve as voltage sensors. Channel opening, inactivation, and recovery are tightly regulated by conformational changes in these domains. Mammalian genomes encode several similar alpha subunits (Nav1.1–Nav1.9), with tissue-specific expression and functional properties. These subunits are essential for normal electrical activity and are common molecular targets for drugs treating epilepsy, arrhythmias, pain, and other disorders. Dysfunction or genetic mutation in these subunits can cause severe neurological or cardiac diseases, making them key targets for therapy and biomarker development.

Other names

VGSC alpha subunitNav alpha subunitSodium channel alpha subunitSCN1A, SCN2A, SCN3A, SCN4A, etc. (gene symbols for different subtypes)Voltage-dependent sodium channel alpha subunitSodium channel protein type x subunit alpha (where x = 1–9, depending on tissue expression)

Channel blockade (inhibition of sodium influx); Stabilization of inactivated state; Modulation of channel gating kinetics; Allosteric modulation by toxins (changing activation/inactivation)