Enables sodium ion binding activity and voltage-gated sodium channel activity. Involved in nervous system development; neuronal action potential; and sodium ion transport. Located in axon initial segment and node of Ranvier. Part of voltage-gated sodium channel complex. Is active in glutamatergic synapse; parallel fiber to Purkinje cell synapse; and synaptic membrane. Biomarker of congestive heart failure. Human ortholog(s) of this gene implicated in benign familial infantile seizures 5 and developmental and epileptic encephalopathy 13. Orthologous to human SCN8A (sodium voltage-gated channel alpha subunit 8); INTERACTS WITH (+)-pilocarpine; (+)-trans-(S)-allethrin; 2,3,7,8-tetrachlorodibenzodioxine.
Na+ channel; naCh6; peripheral nerve protein type 4; PN4; sodium channel 6; sodium channel protein type 8 subunit alpha; sodium channel protein type VIII subunit alpha; sodium channel voltage-gated type VIII alpha polypeptide; sodium channel, voltage gated, type VIII, alpha subunit; sodium channel, voltage-gated, type 8, alpha polypeptide; sodium channel, voltage-gated, type 8, alpha subunit; sodium channel, voltage-gated, type VIII, alpha; sodium channel, voltage-gated, type VIII, alpha polypeptide; voltage-gated sodium channel subunit alpha Nav1.6
bioallethrin affects the reaction [[SCN2B protein co-treated with SCN1B protein co-treated with SCN8A protein mutant form] results in increased transport of Sodium]
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of SCN8A mRNA, [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in decreased expression of SCN8A mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of SCN8A mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in decreased expression of SCN8A mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of SCN8A mRNA, [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in decreased expression of SCN8A mRNA
[NOG protein co-treated with p-Chloromercuribenzoic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1, 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of SCN8A mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in decreased expression of SCN8A mRNA, [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in decreased expression of SCN8A mRNA
[NOG protein co-treated with p-Chloromercuribenzoic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1, 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of SCN8A mRNA
[perfluorooctane sulfonic acid co-treated with Cellulose] results in increased expression of SCN8A mRNA, [perfluorooctane sulfonic acid co-treated with Pectins] results in increased expression of SCN8A mRNA
[NOG protein co-treated with p-Chloromercuribenzoic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1, 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of SCN8A mRNA
[Tetrodotoxin results in decreased activity of [SCN8A protein co-treated with SCN9A protein]] which affects the transport of Sodium, Tetrodotoxin inhibits the reaction [SCN8A protein results in increased transport of Sodium]
Ankyrin-G coordinates assembly of the spectrin-based membrane skeleton, voltage-gated sodium channels, and L1 CAMs at Purkinje neuron initial segments.