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Article: Regulation of transactivation-independent proapoptotic activity of p53 by FOXO3a

TitleRegulation of transactivation-independent proapoptotic activity of p53 by FOXO3a
Authors
KeywordsApoptosis
Issue Date2006
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2006, v. 103, n. 24, p. 9051-9056 How to Cite?
AbstractThe tumor suppressor p53 can trigger cell death independently of its transcriptional activity through subcellular translocation and activation of proapoptotic Bcl-2 family members. The regulation of such activity of endogenous p53 in response to stress remains largely unknown. Here we show that nuclear, activated FOXO3a could impair p53 transcriptional activity. However, activation of FOXO3a either on serum starvation or by expressing a constitutively active form of FOXO3a could induce p53-dependent apoptosis, even in cells bearing a transcriptionally inactive form of p53. Furthermore, FOXO3a could promote p53 cytoplasmic accumulation by increasing its association with nuclear exporting machinery. Our data also suggest that PUMA and Bax are required for p53-dependent apoptosis in manner that is independent of p53 transcriptional activity. © 2006 by The National Academy of Sciences of the USA apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/292193
ISSN
2020 Impact Factor: 11.205
2020 SCImago Journal Rankings: 5.011
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYou, Han-
dc.contributor.authorYamamoto, Kazuo-
dc.contributor.authorMak, Tak Wah-
dc.date.accessioned2020-11-17T14:55:57Z-
dc.date.available2020-11-17T14:55:57Z-
dc.date.issued2006-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2006, v. 103, n. 24, p. 9051-9056-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/292193-
dc.description.abstractThe tumor suppressor p53 can trigger cell death independently of its transcriptional activity through subcellular translocation and activation of proapoptotic Bcl-2 family members. The regulation of such activity of endogenous p53 in response to stress remains largely unknown. Here we show that nuclear, activated FOXO3a could impair p53 transcriptional activity. However, activation of FOXO3a either on serum starvation or by expressing a constitutively active form of FOXO3a could induce p53-dependent apoptosis, even in cells bearing a transcriptionally inactive form of p53. Furthermore, FOXO3a could promote p53 cytoplasmic accumulation by increasing its association with nuclear exporting machinery. Our data also suggest that PUMA and Bax are required for p53-dependent apoptosis in manner that is independent of p53 transcriptional activity. © 2006 by The National Academy of Sciences of the USA apoptosis.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.subjectApoptosis-
dc.titleRegulation of transactivation-independent proapoptotic activity of p53 by FOXO3a-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.0600889103-
dc.identifier.pmid16757565-
dc.identifier.pmcidPMC1482564-
dc.identifier.scopuseid_2-s2.0-33745163907-
dc.identifier.volume103-
dc.identifier.issue24-
dc.identifier.spage9051-
dc.identifier.epage9056-
dc.identifier.isiWOS:000238369100029-
dc.identifier.issnl0027-8424-

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