Phosphatase and tensin homologue deleted on chromosome 10: extending its PTENtacles.

Phosphatase and tensin homologue deleted on chromosome 10: extending its PTENtacles.
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DOI:
10.1016/j.biocel.2008.09.022
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发表时间:
2009-04
影响因子:
4
通讯作者:
Stiles, Bangyan L.
Stiles, Bangyan L.
中科院分区:
生物学2区
文献类型:
--
作者:
Stiles, Bangyan L.

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Since its discovery in 1997, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) has become one of the most important molecules in tumor biology. Mutations, deletions or dysregulation of PTEN is found in many human tumors. Recent studies have extended the reach of PTEN to include diabetes and neurological diseases such as Parkinson’s and Autism. In this review, we summarize the traditionally characterized function of PTEN as the lipid phosphatase that dephosphorylates PI-3,4,5-P3, and several other newly discovered functions. The inhibition of the phosphatidylinositol-3-kinase (PI3K)/AKT signaling pathway may account for most of PTEN’s tumor suppressing function. However, other growth inhibiting functions of PTEN may not involve this pathway. PTEN can also inhibit growth through its protein phosphatase activity and in ways not related to its enzymatic activity at all. We survey the many functions and biochemical interactions of PTEN in cytoplasm, the nucleus and throughout the cell in this paper.
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