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ONLINEISSN:1347-5215
PRINTISSN:0918-6158
Biological & Pharmaceutical Bulletin
Vol. 30 (2007) , No. 9 1624
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PTEN: Its Deregulation and Tumorigenesis
Tomohiko Maehama1)
1) Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
(Received February 27, 2007)
The tumor suppressor phosphatase and tensin homolog (PTEN) functions as a phosphoinositide 3-phosphatase, that antagonizes phosphatidylinositol 3-kinase action, and negatively regulates cell proliferation and survival signals. Inactivation of PTEN by loss-of-function mutations gives rise to deregulated hyperproliferation of cells, leading to oncogenic transformation. Recent studies have identified a number of upstream regulatory factors for PTEN and unveiled that the impairment in the PTEN regulatory system potentially becomes a causal factor for oncogenic transformation of cells. This article will review the PTEN inactivation mechanism which is linked to human tumorigenesis, particularly focusing on recent research progress in PTEN regulators.
Key wordsphosphoinositide; tumor suppressor; phosphatase

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To cite this article:
Tomohiko Maehama, “PTEN: Its Deregulation and Tumorigenesis”, Biol. Pharm. Bull., Vol. 30, 1624-1627 (2007) .

doi:10.1248/bpb.30.1624
JOI  JST.JSTAGE/bpb/30.1624
(c) 2007 The Pharmaceutical Society of Japan



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