| Literature DB >> 24656806 |
Benjamin D Hopkins1, Cindy Hodakoski1, Douglas Barrows1, Sarah M Mense1, Ramon E Parsons2.
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.Entities:
Keywords: PI3K signaling; PTEN; PTEN-Long
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Year: 2014 PMID: 24656806 PMCID: PMC4043120 DOI: 10.1016/j.tibs.2014.02.006
Source DB: PubMed Journal: Trends Biochem Sci ISSN: 0968-0004 Impact factor: 13.807