| First Author | Arakawa-Takeuchi S | Year | 2010 |
| Journal | FEBS Lett | Volume | 584 |
| Issue | 13 | Pages | 2779-85 |
| PubMed ID | 20466002 | Mgi Jnum | J:161318 |
| Mgi Id | MGI:4457985 | Doi | 10.1016/j.febslet.2010.05.005 |
| Citation | Arakawa-Takeuchi S, et al. (2010) Mammalian target of rapamycin complex 1 signaling opposes the effects of anchorage loss, leading to activation of Cdk4 and Cdc6 stabilization. FEBS Lett 584(13):2779-85 |
| abstractText | When deprived of an anchorage to the extracellular matrix, fibroblasts arrest in the G(1) phase with inactivation of Cdk4/6 and Cdk2 and destruction of Cdc6, the assembler of prereplicative complexes essential for S phase onset. How cellular anchorages control these kinases and Cdc6 stability is poorly understood. Here, we report that in rat embryonic fibroblasts, activation of mammalian target of rapamycin complex 1 by a Tsc2 mutation or overexpression of a constitutively active mutant Rheb overrides the absence of the anchorage and stabilizes Cdc6 at least partly via activating Cdk4/6 that induces Emi1, an APC/C(Cdh1) ubiquitin ligase inhibitor. |
