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Sci. Signal., 8 January 2013
Vol. 6, Issue 257, p. pe1
[DOI: 10.1126/scisignal.2003864]

PERSPECTIVES

The Akt DUBbed InAktive

Kui Lin*

Department of Translational Oncology, Research Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.

Abstract: Akt is a central node in the phosphoinositide-3 kinase–Akt–mammalian target of rapamycin pathway and is activated by a multistep process in response to growth factor stimulation. An additional layer of posttranslational modification has emerged as a new paradigm in the regulation of Akt. The identification of an E3 ligase for Lys63-linked ubiquitination of Akt has now been complemented with the discovery of the tumor suppressor cylindromatosis as a deubiquitinating enzyme (DUB) for Akt. Thus, like phosphorylation and dephosphorylation, cycles of ubiquitination and deubiquitination provide additional on-off switches that keep Akt activity in balance, and disturbances in this balance have pathological consequences.

*Corresponding author. E-mail, klin{at}gene.com

Citation: K. Lin, The Akt DUBbed InAktive. Sci. Signal. 6, pe1 (2013).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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W. Li, C. Peng, M.-H. Lee, D. Lim, F. Zhu, Y. Fu, G. Yang, Y. Sheng, L. Xiao, X. Dong, et al. (2013)
Cancer Res. 73, 6938-6950
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