| First Author | Morel C | Year | 2009 |
| Journal | Mol Cell Biol | Volume | 29 |
| Issue | 14 | Pages | 3845-52 |
| PubMed ID | 19433446 | Mgi Jnum | J:150145 |
| Mgi Id | MGI:3849790 | Doi | 10.1128/MCB.00279-09 |
| Citation | Morel C, et al. (2009) Mcl-1 integrates the opposing actions of signaling pathways that mediate survival and apoptosis. Mol Cell Biol 29(14):3845-52 |
| abstractText | Mcl-1 is a member of the Bcl2-related protein family that is a critical mediator of cell survival. Exposure of cells to stress causes inhibition of Mcl-1 mRNA translation and rapid destruction of Mcl-1 protein by proteasomal degradation mediated by a phosphodegron created by glycogen synthase kinase 3 (GSK3) phosphorylation of Mcl-1. Here we demonstrate that prior phosphorylation of Mcl-1 by the c-Jun N-terminal protein kinase (JNK) is essential for Mcl-1 phosphorylation by GSK3. Stress-induced Mcl-1 degradation therefore requires the coordinated activity of JNK and GSK3. Together, these data establish that Mcl-1 functions as a site of signal integration between the proapoptotic activity of JNK and the prosurvival activity of the AKT pathway that inhibits GSK3. |
