Akt Phosphorylates the Transcriptional Repressor Bmi1 to Block Its Effects on the Tumor-Suppressing Ink4a-Arf Locus

Yan Liu,* Fan Liu, Hao Yu, Xinyang Zhao, Goro Sashida, Anthony Deblasio, Michael Harr, Qing-Bai She, Zhenbang Chen, Hui-Kuan Lin, Silvana Di Giandomenico, Shannon E. Elf, Youyang Yang, Yasuhiko Miyata, Gang Huang, Silvia Menendez, Ingo K. Mellinghoff, Neal Rosen, Pier Paolo Pandolfi, Cyrus V. Hedvat, Stephen D. Nimer*

*To whom correspondence should be addressed. E-mail: liu219{at}iupui.edu (Y.L.); snimer{at}med.miami.edu (S.D.N.)

This PDF file includes:

• Fig. S1. Akt phosphorylates Bmi1 in cells.
• Fig. S2. Knockdown of Bmi1 in wild-type MEFs with RNA interference.
• Fig. S3. The Bmi1-S316A mutant enhances tumor formation in nude mice.
• Fig. S4. Phosphorylated Bmi1 is detectable in human diffuse large B cell lymphoma samples.
• Fig. S5. The PI3K-Akt signaling pathway does not affect PRC1 complex formation.
• Fig. S6. Subcellular localization of Bmi1 in U2OS cells after serum or IGF exposure.
• Fig. S7. ChIP assays of the Ink4a-Arf locus in MEFs.

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© 2012 American Association for the Advancement of Science