Pub. Date : 2012 Jan 15
PMID : 22024133
7 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Vinblastine treatment of KB-3 cells initially resulted in a phosphatase-sensitive mobility shift in Mcl-1 and then subsequent loss of Mcl-1 protein expression which was prevented by MG132, suggesting that phosphorylation triggered proteosome-mediated degradation. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 2 | Vinblastine treatment of KB-3 cells initially resulted in a phosphatase-sensitive mobility shift in Mcl-1 and then subsequent loss of Mcl-1 protein expression which was prevented by MG132, suggesting that phosphorylation triggered proteosome-mediated degradation. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 3 | Vinblastine treatment caused degradation of Mcl-1 in cells in which apoptosis was blocked by Bcl-xL overexpression, indicating that Mcl-1 degradation was not a consequence of apoptosis. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 4 | Vinblastine treatment caused degradation of Mcl-1 in cells in which apoptosis was blocked by Bcl-xL overexpression, indicating that Mcl-1 degradation was not a consequence of apoptosis. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 5 | A partial reversible phosphorylation of Mcl-1 was observed in synchronized cells traversing mitosis, whereas more extensive phosphorylation and subsequent degradation of Mcl-1 was observed if synchronized cells were treated with vinblastine. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 6 | Mcl-1 phosphorylation closely paralleled cyclin B expression, and specific cyclin-dependent kinase (Cdk) inhibitors blocked vinblastine-induced Mcl-1 phosphorylation, its subsequent degradation, and improved cell viability after mitotic arrest. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 7 | Mcl-1 phosphorylation closely paralleled cyclin B expression, and specific cyclin-dependent kinase (Cdk) inhibitors blocked vinblastine-induced Mcl-1 phosphorylation, its subsequent degradation, and improved cell viability after mitotic arrest. | Vinblastine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |