Send us a Message



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

GENE - CHEMICAL INTERACTIONS REPORT

RGD ID: 70500
Species: Rattus norvegicus
RGD Object: Gene
Symbol: Mapk1
Name: mitogen activated protein kinase 1
Acc ID: CHEBI:34385
Term: 4-aminopyridine
Definition: An aromatic amine that is pyridine bearing a single amino substituent at position 4. An orphan drug in the US, it is used to improve walking in adults with multiple sclerosis.
Chemical ID: MESH:D015761
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)
Mapk1increases phosphorylationEXP 6480464CTD4-Aminopyridine results in increased phosphorylation of MAPK1 protein

PMID:22759588 PMID:28132918
Mapk1multiple interactionsEXP 6480464CTD2-2-amino-3-methoxyphenyl-4H-1-benzopyran-4-one inhibits the reaction [4-Aminopyridine results in increased phosphorylation of MAPK1 protein] [4-Aminopyridine co-treated with Calcium Chloride] results in increased phosphorylation of MAPK1 protein ciproxifan inhibits the reaction [4-Aminopyridine results in increased phosphorylation of MAPK1 protein] hispidulin inhibits the reaction [4-Aminopyridine results in increased phosphorylation of MAPK1 protein] typhaneoside inhibits the reaction [[4-Aminopyridine co-treated with Calcium Chloride] results in increased phosphorylation of MAPK1 protein]

PMID:22759588 PMID:28132918 PMID:33621091
Mapk1multiple interactionsISORGD:7325036480464CTD[Bicuculline co-treated with 4-Aminopyridine] results in increased activity of and results in increased phosphorylation of MAPK1 protein Dizocilpine Maleate inhibits the reaction [[Bicuculline co-treated with 4-Aminopyridine] results in increased activity of and results in increased phosphorylation of MAPK1 protein]

PMID:19911010
Go Back to source page   Continue to Ontology report