Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 19 March 2002
Vol. 2002, Issue 124, p. tw111
[DOI: 10.1126/stke.2002.124.tw111]


Development Akt-ing Against a Loss

Mutations in the tumor suppressor protein PTEN occur in a variety of cancers. Its major enzymatic activity is to dephosphorylate phosphoinositides, including phosphoinositide-3,4,5-trisphosphate (PIP3). In the absence of PTEN, cellular levels of PIP3 increase, which result in overgrowth phenotypes and lethality in Drosophila larvae. However, PIP3 binds to numerous signaling molecules, and so it is not clear if there is a specific interaction that loss of PTEN function primarily affects. Stocker et al. show that flies can live in the absence of PTEN if the interaction of PIP3 with the serine-threonine kinase Akt is decreased through a mutation in its PH domain. At least in the fly, Akt appears to be the principal target of PIP3.

H. Stocker, M. Andjelkovic, S. Oldham, M. Laffargue, M. P. Wymann, B. A. Hemmings, E. Hafen, Living with lethal PIP3 levels: Viability of flies lacking PTEN restored by a PH domain mutation in Akt/PKB. Science 295, 2088-2091 (2002). [Abstract] [Full Text]

Citation: Akt-ing Against a Loss. Sci. STKE 2002, tw111 (2002).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882