Enables sodium ion binding activity and voltage-gated sodium channel activity. Involved in behavioral response to formalin induced pain; negative regulation of action potential; and neuronal action potential. Located in axon. Part of voltage-gated sodium channel complex. Human ortholog(s) of this gene implicated in erythromelalgia and paroxysmal extreme pain disorder. Orthologous to human SCN9A (sodium voltage-gated channel alpha subunit 9); INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; 2,3,7,8-Tetrachlorodibenzofuran; 6-propyl-2-thiouracil.
[NOG protein co-treated with Valproic 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 SCN9A mRNA
[NOG protein co-treated with Valproic 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 SCN9A mRNA
[Tetrodotoxin results in decreased activity of [SCN8A protein co-treated with SCN9A protein]] which affects the transport of Sodium, Tetrodotoxin inhibits the reaction [SCN9A protein results in increased transport of Sodium]
[Tetrodotoxin results in decreased activity of [SCN8A protein co-treated with SCN9A protein]] which affects the transport of Sodium, Tetrodotoxin inhibits the reaction [SCN9A protein results in increased transport of Sodium]
[NOG protein co-treated with Valproic 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 SCN9A mRNA
Rat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers.