Sci. Signal., 23 October 2012
Silencing the SilencerThe 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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Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882