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Trends Biochem Sci. 2014 Apr;39(4):183-90. doi: 10.1016/j.tibs.2014.02.006. Epub 2014 Mar 18.

PTEN function: the long and the short of it.

Author information

1
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, USA.
2
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, USA. Electronic address: ramon.parsons@mssm.edu.

Abstract

Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a phosphatase that is frequently altered in cancer. PTEN has phosphatase-dependent and -independent roles, and genetic alterations in PTEN lead to deregulation of protein synthesis, the cell cycle, migration, growth, DNA repair, and survival signaling. PTEN localization, stability, conformation, and phosphatase activity are controlled by an array of protein-protein interactions and post-translational modifications. Thus, PTEN-interacting and -modifying proteins have profound effects on the tumor suppressive functions of PTEN. Moreover, recent studies identified mechanisms by which PTEN can exit cells, via either exosomal export or secretion, and act on neighboring cells. This review focuses on modes of PTEN protein regulation and ways in which perturbations in this regulation may lead to disease.

KEYWORDS:

PI3K signaling; PTEN; PTEN-Long

PMID:
24656806
PMCID:
PMC4043120
DOI:
10.1016/j.tibs.2014.02.006
[Indexed for MEDLINE]
Free PMC Article

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