Striking the balance between PTEN and PDK1: it all depends on the cell context
- 1Department of Pathology and Laboratory Medicine, the Henry Singleton Brain Tumor Program at the David Geffen University of California at Los Angeles School of Medicine, Los Angeles, California 90095, USA;
- 2Department of Neurology, the Henry Singleton Brain Tumor Program at the David Geffen University of California at Los Angeles School of Medicine, Los Angeles, Calforinia 90095, USA;
- 3Department of Molecular and Medical Pharmacology, the Henry Singleton Brain Tumor Program at the David Geffen University of California at Los Angeles School of Medicine, Los Angeles, Californai 90095, USA
Abstract
The phosphatidyl-inosital-3 kinase (PI3K) signaling pathway is critical for normal brain development and function and is commonly hyperactivated in brain cancer. The PTEN (phosphatase and tensin homolog deleted on chromosome 10) tumor suppressor protein and phosphate-depended kinase 1 (PDK-1) are critical regulators of this pathway. In the July 15, 2009, issue of Genes & Development, Chalhoub and colleagues (pp. 1619–1624) demonstrate PDK1-dependent and PDK1-independent effects of conditional PTEN deletion in the brain, and they identify cell type-specific differences in feedback regulation of the PI3K pathway. These studies provide important insights as to how neurons and glia may differentially regulate PI3K signaling, yielding intriguing clues about targeting PTEN-deficient brain cancers.
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↵1 Corresponding author.
E-MAIL pmischel{at}mednet.ucla.edu; FAX (310) 794-4161.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1832909.
- Copyright © 2009 by Cold Spring Harbor Laboratory Press
