Send us a Message



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

GENE - CHEMICAL INTERACTIONS REPORT

RGD ID: 620360
Species: Rattus norvegicus
RGD Object: Gene
Symbol: Nfe2l2
Name: NFE2 like bZIP transcription factor 2
Acc ID: CHEBI:134301
Term: salvianolic acid B
Definition: A member of the class of 1-benzofurans that is an antioxidant and free radical scavenging compound extracted from S. miltiorrhiza
Chemical ID: MESH:C076944
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)
Nfe2l2multiple interactionsEXP 6480464CTDsalvianolic acid B inhibits the reaction [Cisplatin results in decreased expression of NFE2L2 protein]PMID:33952797
Nfe2l2increases expressionISONfe2l2 (Mus musculus)6480464CTDsalvianolic acid B results in increased expression of NFE2L2 proteinPMID:24991814
Nfe2l2multiple interactionsISONfe2l2 (Mus musculus)6480464CTDNFE2L2 protein affects the reaction [salvianolic acid B inhibits the reaction [Lipopolysaccharides results in increased secretion of IL1B protein]]; NFE2L2 protein affects the reaction [salvianolic acid B inhibits the reaction [Lipopolysaccharides results in increased secretion of TNF protein]]; NFE2L2 protein affects the reaction [salvianolic acid B results in increased expression of GDNF mRNA]; NFE2L2 protein affects the reaction [salvianolic acid B results in increased secretion of GDNF protein]; salvianolic acid B inhibits the reaction [1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine results in decreased expression of NFE2L2 protein]; salvianolic acid B inhibits the reaction [Cisplatin results in decreased expression of NFE2L2 protein]; salvianolic acid B results in increased secretion of and affects the localization of NFE2L2 proteinPMID:24991814 PMID:33952797
Go Back to source page   Continue to Ontology report