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Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation.

DC Field Value Language
dc.contributor.authorJung, MS-
dc.contributor.authorJin, DH-
dc.contributor.authorChae, HD-
dc.contributor.authorKang, S-
dc.contributor.authorKim, SC-
dc.contributor.authorBang, YJ-
dc.contributor.authorChoi, TS-
dc.contributor.authorChoi, KS-
dc.contributor.authorShin, DY-
dc.date.accessioned2011-07-14T05:00:36Z-
dc.date.available2011-07-14T05:00:36Z-
dc.date.issued2004-
dc.identifier.issn0021-9258-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3355-
dc.description.abstractIn this study, we describe novel functions of the anti-apoptotic Bcl-2 family proteins. Bcl-x(L) and E1B-19K were found to inhibit p53-induced irreversible growth arrest and senescence, but not to inhibit transient growth arrest, implying that Bcl-x(L) and E1B-19K are specifically involved in senescence without participating in growth arrest. We provide several lines of evidences showing that the functions of Bcl-x(L) and E1B-19K to prevent generation of reactive oxygen species (ROS) are important to inhibit senescence induction. First, we found that that ROS are increased during p53-induced senescence. Moreover, Bcl-x(L) and E1B-19K inhibit this p53-induced ROS generation. Second, antioxidants prevent the induction of senescence and ROS by p53, but not the persistence of the senescence phenotype. Third, the anti-senescence functions of Bcl-x(L) and E1B-19K were suppressed by adding exogenous ROS. These results suggest that Bcl-x(L) and E1B-19K inhibit senescence induction by preventing ROS generation. Furthermore, p38 kinase was found to be activated during p53-induced senescence, but not in cells expressing Bcl-x(L) or E1B-19K, or in cells treated with anti-oxidants. Consistently, a chemical inhibitor of p38 kinase, SB203580, was found to inhibit p53-induced senescence, but only when treated before the cellular commitment to senescence, implying that p38 kinase is necessary for senescence induction. Therefore, Bcl-x(L) and E1B-19K inhibit p53-induced senescence by preventing ROS generation, which in turn leads to the activation of p38 kinase. These results also suggest that the oncogenic potential of Bcl-2 is due to its ability to inhibit senescence as well as apoptosis.-
dc.language.isoen-
dc.subject.MESHAdenovirus E1B Proteins-
dc.subject.MESHAntioxidants-
dc.subject.MESHApoptosis-
dc.subject.MESHBromodeoxyuridine-
dc.subject.MESHCell Aging-
dc.subject.MESHCell Division-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHHumans-
dc.subject.MESHImidazoles-
dc.subject.MESHImmunoblotting-
dc.subject.MESHMitogen-Activated Protein Kinases-
dc.subject.MESHOxidants-
dc.subject.MESHPhenotype-
dc.subject.MESHPhosphorylation-
dc.subject.MESHProtein Binding-
dc.subject.MESHProto-Oncogene Proteins c-bcl-2-
dc.subject.MESHPyridines-
dc.subject.MESHReactive Oxygen Species-
dc.subject.MESHTime Factors-
dc.subject.MESHTumor Suppressor Protein p53-
dc.subject.MESHbcl-X Protein-
dc.subject.MESHbeta-Galactosidase-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases-
dc.titleBcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation.-
dc.typeArticle-
dc.identifier.pmid14764594-
dc.identifier.urlhttp://www.jbc.org/cgi/pmidlookup?view=long&pmid=14764594-
dc.contributor.affiliatedAuthor최, 경숙-
dc.type.localJournal Papers-
dc.identifier.doi10.1074/jbc.M305015200-
dc.citation.titleThe Journal of biological chemistry-
dc.citation.volume279-
dc.citation.number17-
dc.citation.date2004-
dc.citation.startPage17765-
dc.citation.endPage17771-
dc.identifier.bibliographicCitationThe Journal of biological chemistry, 279(17). : 17765-17771, 2004-
dc.identifier.eissn1083-351X-
dc.relation.journalidJ000219258-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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