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Sci. Signal., 23 October 2012
Vol. 5, Issue 247, p. ra77
[DOI: 10.1126/scisignal.2003199]


Editor's Summary

Silencing the Silencer
The Polycomb group protein Bmi1 transcriptionally silences the Ink4a-Arf locus and thus decreases the abundance of the tumor suppressor proteins p16 and p19. Liu et al. found that phosphorylation of Bmi1 by the kinase Akt causes it to dissociate from the Ink4a-Arf locus, which results in increased abundance of p16 and p19 that decreases cellular proliferation, tumor growth, and self-renewal of stem and progenitor cells. Thus, Akt, which is typically activated downstream of growth-promoting signals, can mediate a feedback loop that ultimately attenuates these growth signals.

Citation: Y. Liu, F. Liu, H. Yu, X. Zhao, G. Sashida, A. Deblasio, M. Harr, Q.-B. She, Z. Chen, H.-K. Lin, S. Di Giandomenico, S. E. Elf, Y. Yang, Y. Miyata, G. Huang, S. Menendez, I. K. Mellinghoff, N. Rosen, P. P. Pandolfi, C. V. Hedvat, S. D. Nimer, Akt Phosphorylates the Transcriptional Repressor Bmi1 to Block Its Effects on the Tumor-Suppressing Ink4a-Arf Locus. Sci. Signal. 5, ra77 (2012).

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Mitogen-activated Protein Kinase Signaling Mediates Phosphorylation of Polycomb Ortholog Cbx7.
H.-a. Wu, J. L. Balsbaugh, H. Chandler, A. Georgilis, H. Zullow, J. Shabanowitz, D. F. Hunt, J. Gil, G. Peters, and E. Bernstein (2013)
J. Biol. Chem. 288, 36398-36408
   Abstract »    Full Text »    PDF »
Lineage-inappropriate PAX5 expression in t(8;21) acute myeloid leukemia requires signaling-mediated abrogation of polycomb repression.
D. Ray, S. Y. Kwon, H. Tagoh, O. Heidenreich, A. Ptasinska, and C. Bonifer (2013)
Blood 122, 759-769
   Abstract »    Full Text »    PDF »
Science Signaling Podcast: 23 October 2012.
S. D. Nimer and A. M. VanHook (2012)
Science Signaling 5, pc23
   Abstract »    Full Text »

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