The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Regulation of G1progression by the PTEN tumor suppressor protein is linked to inhibition of the phosphatidylinositol 3-kinase/Akt pathway
Open accessAbstract
PTEN/MMAC1 is a tumor suppressor gene located on chromosome 10q23. Inherited PTEN/MMAC1 mutations are associated with a cancer predisposition syndrome known as Cowden’s disease. Somatic mutation of PTEN has been found in a number of malignancies, including glioblastoma, melanoma, and carcinoma of the prostate and endometrium. The protein product (PTEN) encodes a dual-specificity protein phosphatase and in addition can dephosphorylate certain lipid substrates. Herein, we show that PTEN protein induces a G 1 block when reconstituted in PTEN-null cells. A PTEN mutant associated with Cowden’s disease (PTEN;G129E) has protein phosphatase activity yet is defective in dephosphorylating inositol 1,3,4,5-tetrakisphosphate in vitro and fails to arrest cells in G 1. These data suggest a link between induction of a cell-cycle block by PTEN and its ability to dephosphorylate,in vivo,phosphatidylinositol 3,4,5-trisphosphate. In keeping with this notion, PTEN can inhibit the phosphatidylinositol 3,4,5-trisphosphate-dependent Akt kinase, a downstream target of phosphatidylinositol 3-kinase, and constitutively active, but not wild-type, Akt overrides a PTEN G 1 arrest. Finally, tumor cells lacking PTEN contain high levels of activated Akt, suggesting that PTEN is necessary for the appropriate regulation of the phosphatidylinositol 3-kinase/Akt pathway.
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Metadata
- Authors
- Ramaswamy, S., Nakamura, N., Vazquez, F., Batt, D. B., Perera, S., Roberts, T. M., & Sellers, W. R.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-03-02
- Volume
- 96
- Issue
- 5
- Pages
- 2110-2115
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2070942270
- Cited by
- 575
- References
- 2
- FWCI
- 12.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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