File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Modulation of cellular apoptotic potential: Contributions to oncogenesis

TitleModulation of cellular apoptotic potential: Contributions to oncogenesis
Authors
KeywordsPTEN
Apoptosis
PI3'K
Cell survival
Issue Date1999
Citation
Oncogene, 1999, v. 18, n. 45, p. 6094-6103 How to Cite?
AbstractThe importance of apoptosis as a natural means to eliminate unwanted or damaged cells has been realized over the past decade. Many components required to exercise programmed cell death have been identified and shown to pre-exist in most, if not all, cells. Such ubiquity requires that apoptosis be tightly controlled and suggests the propensity of cells to trigger the cellular death machinery can be regulated. Recently, several signaling pathways have been demonstrated to impact the apoptotic potential of cells, most notably the phosphatidylinositol 3' kinase (PI3'K) pathway. The 3' phosphorylated lipid products generated by this enzyme promote activation of a protein-serine kinase, PKB/AKT, which is necessary and sufficient to confer cell PI3'K-dependent survival signals. The relevance of this pathway to human cancer was revealed by the recent finding that the product of the PTEN tumor suppressor gene acts to antagonize PI3'K. This review focuses on the regulation and mechanisms by which PKB activation protects cells and the oncologic consequences of dysregulation of the pathway.
Persistent Identifierhttp://hdl.handle.net/10722/291492
ISSN
2020 Impact Factor: 9.867
2020 SCImago Journal Rankings: 3.395
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorStambolic, Vuk-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorWoodgett, James R.-
dc.date.accessioned2020-11-17T14:54:29Z-
dc.date.available2020-11-17T14:54:29Z-
dc.date.issued1999-
dc.identifier.citationOncogene, 1999, v. 18, n. 45, p. 6094-6103-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/291492-
dc.description.abstractThe importance of apoptosis as a natural means to eliminate unwanted or damaged cells has been realized over the past decade. Many components required to exercise programmed cell death have been identified and shown to pre-exist in most, if not all, cells. Such ubiquity requires that apoptosis be tightly controlled and suggests the propensity of cells to trigger the cellular death machinery can be regulated. Recently, several signaling pathways have been demonstrated to impact the apoptotic potential of cells, most notably the phosphatidylinositol 3' kinase (PI3'K) pathway. The 3' phosphorylated lipid products generated by this enzyme promote activation of a protein-serine kinase, PKB/AKT, which is necessary and sufficient to confer cell PI3'K-dependent survival signals. The relevance of this pathway to human cancer was revealed by the recent finding that the product of the PTEN tumor suppressor gene acts to antagonize PI3'K. This review focuses on the regulation and mechanisms by which PKB activation protects cells and the oncologic consequences of dysregulation of the pathway.-
dc.languageeng-
dc.relation.ispartofOncogene-
dc.subjectPTEN-
dc.subjectApoptosis-
dc.subjectPI3'K-
dc.subjectCell survival-
dc.titleModulation of cellular apoptotic potential: Contributions to oncogenesis-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/sj.onc.1203126-
dc.identifier.pmid10557100-
dc.identifier.scopuseid_2-s2.0-0033231188-
dc.identifier.volume18-
dc.identifier.issue45-
dc.identifier.spage6094-
dc.identifier.epage6103-
dc.identifier.isiWOS:000083447100003-
dc.identifier.issnl0950-9232-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats