Enables calmodulin binding activity. Involved in cellular response to antibiotic; nervous system development; and response to pyrethroid. Located in axon and neuronal cell body. Human ortholog(s) of this gene implicated in developmental and epileptic encephalopathy 62 and familial focal epilepsy with variable foci 4. Orthologous to human SCN3A (sodium voltage-gated channel alpha subunit 3); INTERACTS WITH 17alpha-ethynylestradiol; 2,2',4,4'-Tetrabromodiphenyl ether; 2,3,7,8-tetrachlorodibenzodioxine.
LOC100360249; Nav1.3; rCG26412-like; SCIII; Scn2a; sodium channel protein brain III subunit alpha; sodium channel protein type 3 subunit alpha; sodium channel protein type 3 subunit alpha-like; sodium channel protein type III subunit alpha; sodium channel protein, brain III subunit alpha; sodium channel, voltage-gated, type 3, alpha subunit; sodium channel, voltage-gated, type III, alpha; sodium channel, voltage-gated, type III, alpha polypeptide; sodium channel, voltage-gated, type III, alpha subunit; voltage-gated sodium channel subtype III; voltage-gated sodium channel subunit alpha Nav1.3
[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 more ...
[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 more ...
2,3,5,6-tetrafluoro-4-methylbenzyl (Z)-(1RS)-cis-3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclopropanecarboxylate inhibits the reaction [[SCN3A protein co-treated with SCN2B protein co-treated with SCN1B protein] more ...
[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 more ...
[NOG protein co-treated with Vorinostat 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 more ...
Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury.
Deglycosylation altered the gating properties of rNav1.3: glycosylation/deglycosylation homeostasis probably complicates the functional regulation of voltage-gated sodium channel.