Degradation of Mcl-1 by beta-TrCP mediates glycogen synthase kinase 3-induced tumor suppression and chemosensitization.

@article{Ding2007DegradationOM,
  title={Degradation of Mcl-1 by beta-TrCP mediates glycogen synthase kinase 3-induced tumor suppression and chemosensitization.},
  author={Qingqing Ding and Xianghuo He and J -M. Hsu and Weiya Xia and Chun-Te Chen and L Y Li and Dung-Fang Lee and J Liu and Qing Zhong and Xiaodong Wang and M -C Hung},
  journal={Molecular and cellular biology},
  year={2007},
  volume={27 11},
  pages={4006-17}
}
Apoptosis is critical for embryonic development, tissue homeostasis, and tumorigenesis and is determined largely by the Bcl-2 family of antiapoptotic and prosurvival regulators. Here, we report that glycogen synthase kinase 3 (GSK-3) was required for Mcl-1 degradation, and we identified a novel mechanism for proteasome-mediated Mcl-1 turnover in which GSK-3beta associates with and phosphorylates Mcl-1 at one consensus motif ((155)STDG(159)SLPS(163)T; phosphorylation sites are in italics), which… CONTINUE READING
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