mTOR and Akt signaling in cancer: SGK cycles in.

Molecular cell ·Vol. 31 ·No. 1 ·2008-07-11 ·Pages 6-8

Toker A

Abstract

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.

MeSH Terms

Cell Cycle Cyclin-Dependent Kinase Inhibitor p27/metabolism Enzyme Activation Humans Immediate-Early Proteins/metabolism Neoplasms/enzymology Phosphatidylinositol 3-Kinases/metabolism Phosphorylation Protein Kinases/metabolism Protein Serine-Threonine Kinases/metabolism Proto-Oncogene Proteins c-akt/metabolism Signal Transduction TOR Serine-Threonine Kinases

Chemicals

Immediate-Early Proteins Cyclin-Dependent Kinase Inhibitor p27 Protein Kinases MTOR protein, human Protein Serine-Threonine Kinases Proto-Oncogene Proteins c-akt TOR Serine-Threonine Kinases serum-glucocorticoid regulated kinase

Authors & Affiliations

1 authors, click to expand affiliations / ORCID

Toker Alex

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. atoker@bidmc.harvard.edu

Article Info

Journal

Molecular cell

Abbr.

Mol Cell

ISSN

1097-4164

DOI

10.1016/j.molcel.2008.06.007

atoker@bidmc.harvard.edu

Published

2008-07-11

Pages

6-8

Language

English

Region

United States

NLM ID

9802571

Subset

Corrections

CommentOn

PMID: 18570873

External Links

PubMed source DOI: 10.1016/j.molcel.2008.06.007 View journal details

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mTOR and Akt signaling in cancer: SGK cycles in.

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