mTOR and Akt signaling in cancer: SGK cycles in.
In a recent issue of Molecular Cell, Hong et al. (2008) describe an alternative mechanism by which mTOR promotes cell-cycle progression; it phosphorylates and activates SGK, which in turn phosphorylates the cell-cycle inhibitor p27, promoting its cytoplasmic retention.
Toker
Alex
A
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. atoker@bidmc.harvard.edu
D002453:Cell Cycle; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism; D004789:Enzyme Activation; D006801:Humans; D017874:Immediate-Early Proteins / Q000378:metabolism*; D009369:Neoplasms / Q000201:enzymology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation; D011494:Protein Kinases / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases; D000099184:Serum-Glucocorticoid Regulated Kinases
D050760:Cyclin-Dependent Kinase Inhibitor p27; D017874:Immediate-Early Proteins; D019869:Phosphatidylinositol 3-Kinases; D011494:Protein Kinases; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D000099184:Serum-Glucocorticoid Regulated Kinases; C546842:MTOR protein, human