Akt phosphorylates the transcriptional repressor bmi1 to block its effects on the tumor-suppressing ink4a-arf locus.

@article{Liu2012AktPT,
  title={Akt phosphorylates the transcriptional repressor bmi1 to block its effects on the tumor-suppressing ink4a-arf locus.},
  author={Yan Liu and Fan Liu and Hao Yu and Xinyang Zhao and Goro Sashida and Anthony Deblasio and Michael W Harr and Qing-Bai She and Zhenbang Chen and Hui-Kuan Lin and Silvana di Giandomenico and Shannon E. Elf and Youyang Yang and Yasuhiko Miyata and Gang Huang and Silvia Men{\'e}ndez and Ingo K. Mellinghoff and Neal Rosen and Pier Paolo Pandolfi and Cyrus V. Hedvat and Stephen Nimer},
  journal={Science signaling},
  year={2012},
  volume={5 247},
  pages={ra77}
}
The Polycomb group protein Bmi1 is a transcriptional silencer of the Ink4a-Arf locus, which encodes the cell cycle regulator p16(Ink4a) and the tumor suppressor p19(Arf). Bmi1 plays a key role in oncogenesis and stem cell self-renewal. We report that phosphorylation of human Bmi1 at Ser³¹⁶ by Akt impaired its function by triggering its dissociation from the Ink4a-Arf locus, which resulted in decreased ubiquitylation of histone H2A and the inability of Bmi1 to promote cellular proliferation and… CONTINUE READING
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