Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

GENE - CHEMICAL INTERACTIONS REPORT

RGD ID: 736507
Species: Mus musculus
RGD Object: Gene
Symbol: Scn8a
Name: sodium channel, voltage-gated, type VIII, alpha
Acc ID: CHEBI:26708
Term: sodium atom
Definition: An alkali metal atom that has formula Na.
Chemical ID: MESH:D012964
Note: Use of the qualifier "multiple interactions" designates that the annotated interaction is comprised of a complex set of reactions and/or regulatory events, possibly involving additional chemicals and/or gene products.
Object SymbolQualifierEvidenceWithReferenceSourceNotesOriginal Reference(s)
Scn8aincreases transportEXP 6480464CTDSCN8A protein results in increased transport of SodiumPMID:16020462
Scn8amultiple interactionsEXP 6480464CTD[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]PMID:16020462 PMID:23382806
Scn8amultiple interactionsISOScn8a (Rattus norvegicus)6480464CTD2,3,5,6-tetrafluoro-4-methylbenzyl (Z)-(1RS)-cis-3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclopropanecarboxylate affects the reaction [[SCN2B protein co-treated with SCN1B protein co-treated with SCN8A protein mutant form] results in increased transport of Sodium]; [SCN2B protein co-treated with SCN1B protein co-treated with SCN8A protein mutant form] results in increased transport of Sodium; [SCN2B protein co-treated with SCN1B protein co-treated with SCN8A protein] results in increased transport of Sodium; bioallethrin affects the reaction [[SCN2B protein co-treated with SCN1B protein co-treated with SCN8A protein mutant form] results in increased transport of Sodium]; decamethrin affects the reaction [[SCN2B protein co-treated with SCN1B protein co-treated with SCN8A protein mutant form] results in increased transport of Sodium]PMID:22465659
Go Back to source page   Continue to Ontology report