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AKT activation in human glioblastomas enhances proliferation via TSC2 and S6 kinase signaling

Riemenschneider, Markus J. ; Betensky, Rebecca A. ; Pasedag, Saskia M. ; Louis, David N.



Abstract

Aberrant AKT (protein kinase B) signaling is common in many cancers, including glioblastoma. Current models suggest that AKT acts directly, or indirectly via the TSC complex, to activate the mammalian target of rapamycin (mTOR) as the main downstream mediator of AKT signaling. mTOR activation results in subsequent activation of S6K and STAT3, as well as suppression (i.e., phosphorylation) of ...

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