Send us a Message



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

GENE - CHEMICAL INTERACTIONS REPORT

RGD ID: 735512
Species: Homo sapiens
RGD Object: Gene
Symbol: MCL1
Name: MCL1 apoptosis regulator, BCL2 family member
Acc ID: CHEBI:47344
Term: alvocidib
Definition: A synthetic dihydroxyflavone that is 5,7-dihydroxyflavone which is substituted by a 3-hydroxy-1-methylpiperidin-4-yl group at position 8 and by a chlorine at the 2' position (the (-)-3S,4R stereoisomer). A cyclin-dependent kinase 9 (CDK9) inhibitor, it has been studied for the treatment of acute myeloid leukaemia, arthritis and atherosclerotic plaque formation.
Chemical ID: MESH:C077990
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)
MCL1affects expressionEXP 6480464CTDalvocidib affects the expression of MCL1 mRNA; alvocidib affects the expression of MCL1 proteinPMID:12429644
MCL1decreases expressionEXP 6480464CTDalvocidib results in decreased expression of MCL1 mRNA; alvocidib results in decreased expression of MCL1 proteinPMID:10887097 PMID:12517783 PMID:12533675 PMID:15972445
MCL1decreases response to substanceEXP 6480464CTDMCL1 results in decreased susceptibility to alvocidibPMID:12429644 PMID:12533675
MCL1multiple interactionsEXP 6480464CTD[alvocidib co-treated with ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate] results in decreased expression of MCL1 protein; [Imatinib Mesylate co-treated with alvocidib] results in decreased expression of MCL1 protein; Epothilones promotes the reaction [alvocidib results in decreased expression of MCL1 mRNA]; Epothilones promotes the reaction [alvocidib results in decreased expression of MCL1 protein]PMID:12231544 PMID:12517783 PMID:15634644
Go Back to source page   Continue to Ontology report