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Article: Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN

TitleNegative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN
Authors
Issue Date1998
Citation
Cell, 1998, v. 95, n. 1, p. 29-39 How to Cite?
AbstractPTEN is a tumor suppressor with sequence homology to protein tyrosine phosphatases and the cytoskeletal protein tensin. mPTEN-mutant mouse embryos display regions of increased proliferation. In contrast, mPTEN-deficient immortalized mouse embryonic fibroblasts exhibit decreased sensitivity to cell death in response to a number of apoptotic stimuli, accompanied by constitutively elevated activity and phosphorylation of protein kinase B/Akt, a crucial regulator of cell survival. Expression of exogenous PTEN in mutant cells restores both their sensitivity to agonist-induced apoptosis and normal pattern of PKB/Akt phosphorylation. Furthermore, PTEN negatively regulates intracellular levels of phosphatidylinositol (3,4,5) trisphosphate in cells and dephosphorylates it in vitro. Our results show that PTEN may exert its role as a tumor suppressor by negatively regulating the Pl3'K/PKB/Akt signaling pathway.
Persistent Identifierhttp://hdl.handle.net/10722/291457
ISSN
2023 Impact Factor: 45.5
2023 SCImago Journal Rankings: 24.342
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorStambolic, Vuk-
dc.contributor.authorSuzuki, Akira-
dc.contributor.authorDe la Pompa, José Lois-
dc.contributor.authorBrothers, Greg M.-
dc.contributor.authorMirtsos, Christine-
dc.contributor.authorSasaki, Takehiko-
dc.contributor.authorRuland, Jurgen-
dc.contributor.authorPenninger, Josef M.-
dc.contributor.authorSiderovski, David P.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:24Z-
dc.date.available2020-11-17T14:54:24Z-
dc.date.issued1998-
dc.identifier.citationCell, 1998, v. 95, n. 1, p. 29-39-
dc.identifier.issn0092-8674-
dc.identifier.urihttp://hdl.handle.net/10722/291457-
dc.description.abstractPTEN is a tumor suppressor with sequence homology to protein tyrosine phosphatases and the cytoskeletal protein tensin. mPTEN-mutant mouse embryos display regions of increased proliferation. In contrast, mPTEN-deficient immortalized mouse embryonic fibroblasts exhibit decreased sensitivity to cell death in response to a number of apoptotic stimuli, accompanied by constitutively elevated activity and phosphorylation of protein kinase B/Akt, a crucial regulator of cell survival. Expression of exogenous PTEN in mutant cells restores both their sensitivity to agonist-induced apoptosis and normal pattern of PKB/Akt phosphorylation. Furthermore, PTEN negatively regulates intracellular levels of phosphatidylinositol (3,4,5) trisphosphate in cells and dephosphorylates it in vitro. Our results show that PTEN may exert its role as a tumor suppressor by negatively regulating the Pl3'K/PKB/Akt signaling pathway.-
dc.languageeng-
dc.relation.ispartofCell-
dc.titleNegative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/S0092-8674(00)81780-8-
dc.identifier.pmid9778245-
dc.identifier.scopuseid_2-s2.0-0032475861-
dc.identifier.volume95-
dc.identifier.issue1-
dc.identifier.spage29-
dc.identifier.epage39-
dc.identifier.isiWOS:000076242300008-
dc.identifier.issnl0092-8674-

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