Send us a Message



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

GENE - CHEMICAL INTERACTIONS REPORT

RGD ID: 1320897
Species: Mus musculus
RGD Object: Gene
Symbol: Ripk1
Name: receptor (TNFRSF)-interacting serine-threonine kinase 1
Acc ID: CHEBI:16236
Term: ethanol
Definition: A primary alcohol that is ethane in which one of the hydrogens is substituted by a hydroxy group.
Chemical ID: MESH:D000431
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)
Ripk1affects expressionEXP 6480464CTDEthanol affects the expression of RIPK1 mRNAPMID:30319688
Ripk1decreases expressionEXP 6480464CTDEthanol results in decreased expression of RIPK1 mRNA; Ethanol results in decreased expression of RIPK1 proteinPMID:26769846
Ripk1multiple interactionsEXP 6480464CTD4-O-methylhonokiol inhibits the reaction [[Ethanol co-treated with Carbon Tetrachloride] results in decreased expression of RIPK1 mRNA]; [Ethanol co-treated with Carbon Tetrachloride] results in decreased expression of RIPK1 mRNAPMID:28689299
Ripk1increases expressionISORIPK1 (Homo sapiens)6480464CTDEthanol results in increased expression of RIPK1 proteinPMID:30853489 PMID:34474091
Ripk1multiple interactionsISORIPK1 (Homo sapiens)6480464CTDEthanol promotes the reaction [RIPK1 protein binds to RIPK3 protein]; Gallic Acid inhibits the reaction [Ethanol results in increased expression of RIPK1 protein]; NFATC4 protein inhibits the reaction [pterostilbene inhibits the reaction [Ethanol results in increased expression of RIPK1 protein]]; pterostilbene inhibits the reaction [Ethanol promotes the reaction [RIPK1 protein binds to RIPK3 protein]]; pterostilbene inhibits the reaction [Ethanol results in increased expression of RIPK1 protein]PMID:30853489 PMID:34474091
Go Back to source page   Continue to Ontology report