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Article: Nucling recruits Apaf-1/pro-caspase-9 complex for the induction of stress-induced apoptosis

TitleNucling recruits Apaf-1/pro-caspase-9 complex for the induction of stress-induced apoptosis
Authors
Issue Date2004
Citation
Journal of Biological Chemistry, 2004, v. 279, n. 39, p. 41131-41140 How to Cite?
AbstractNucling is a novel protein isolated from murine embryonal carcinoma cells with an up-regulated expression during cardiac muscle differentiation. We show here that Nucling was up-regulated by proapoptotic stimuli and important for the induction of apoptosis after cytotoxic stress. We further demonstrated that overexpressed Nucling was able to induce apoptosis. In Nucling-deficient cells, the expression levels of Apaf-1 and cytochrome c, which are the major components of an apoptosis-promoting complex named apoptosome, were both down-regulated under cellular stress. A deficiency of Nucling also conferred resistance to apoptotic stress on the cell. After UV irradiation, Nucling was shown to reside in an Apaf-1/pro-caspase-9 complex, suggesting that Nucling might be a key molecule for the formation and maintenance of this complex. Nucling induced translocation of Apaf-1 to the nucleus, thereby distributing the Nucling/Apaf-1/pro-caspase-9 complex to the nuclear fraction. These findings suggest that Nucling recruits and transports the apoptosome complex during stress-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/291838
ISSN
2020 Impact Factor: 5.157
2023 SCImago Journal Rankings: 1.766
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSakai, Takashi-
dc.contributor.authorLiu, Li-
dc.contributor.authorTeng, Xichuan-
dc.contributor.authorMukai-Sakai, Rika-
dc.contributor.authorShimada, Hidenori-
dc.contributor.authorKaji, Ryuji-
dc.contributor.authorMitani, Tasuku-
dc.contributor.authorMatsumoto, Mitsuru-
dc.contributor.authorToida, Kazunori-
dc.contributor.authorIshimura, Kazunori-
dc.contributor.authorShishido, Yuji-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorFukui, Kiyoshi-
dc.date.accessioned2020-11-17T14:55:13Z-
dc.date.available2020-11-17T14:55:13Z-
dc.date.issued2004-
dc.identifier.citationJournal of Biological Chemistry, 2004, v. 279, n. 39, p. 41131-41140-
dc.identifier.issn0021-9258-
dc.identifier.urihttp://hdl.handle.net/10722/291838-
dc.description.abstractNucling is a novel protein isolated from murine embryonal carcinoma cells with an up-regulated expression during cardiac muscle differentiation. We show here that Nucling was up-regulated by proapoptotic stimuli and important for the induction of apoptosis after cytotoxic stress. We further demonstrated that overexpressed Nucling was able to induce apoptosis. In Nucling-deficient cells, the expression levels of Apaf-1 and cytochrome c, which are the major components of an apoptosis-promoting complex named apoptosome, were both down-regulated under cellular stress. A deficiency of Nucling also conferred resistance to apoptotic stress on the cell. After UV irradiation, Nucling was shown to reside in an Apaf-1/pro-caspase-9 complex, suggesting that Nucling might be a key molecule for the formation and maintenance of this complex. Nucling induced translocation of Apaf-1 to the nucleus, thereby distributing the Nucling/Apaf-1/pro-caspase-9 complex to the nuclear fraction. These findings suggest that Nucling recruits and transports the apoptosome complex during stress-induced apoptosis.-
dc.languageeng-
dc.relation.ispartofJournal of Biological Chemistry-
dc.titleNucling recruits Apaf-1/pro-caspase-9 complex for the induction of stress-induced apoptosis-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.M402902200-
dc.identifier.pmid15271982-
dc.identifier.scopuseid_2-s2.0-4644292464-
dc.identifier.volume279-
dc.identifier.issue39-
dc.identifier.spage41131-
dc.identifier.epage41140-
dc.identifier.isiWOS:000223916800112-
dc.identifier.issnl0021-9258-

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