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Sci. Signal., 21 April 2009
Vol. 2, Issue 67, p. pe26
[DOI: 10.1126/scisignal.267pe26]

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Akt Demoted in Glioblastoma

Peter K. Vogt* and Jonathan R. Hart

The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

Abstract: In glioblastomas, an Akt-independent, PTEN (phosphatase and tensin homolog deleted on chromosome ten)–regulated signaling pathway links EGFR (epidermal growth factor receptor) to the phosphorylation of TOR (target of rapamycin) and of the ribosomal protein S6 and to the control of cell replication. Although PKC{alpha} (protein kinase C{alpha}) has been identified as an essential component, the detailed wiring of this previously unexplored noncanonical pathway remains to be worked out.

* To whom correspondence should be addressed. E-mail, pkvogt{at}scripps.edu

Citation: P. K. Vogt, J. R. Hart, Akt Demoted in Glioblastoma. Sci. Signal. 2, pe26 (2009).

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