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dc.contributor.authorGranja, Aitor G.-
dc.contributor.authorNogal París, María Luisa-
dc.contributor.authorHurtado, Carolina-
dc.contributor.authorSalas, José-
dc.contributor.authorSalas, María Luisa-
dc.contributor.authorCarrascosa, Ángel L.-
dc.contributor.authorRevilla Novella, Yolanda-
dc.date.accessioned2008-11-10T15:47:04Z-
dc.date.available2008-11-10T15:47:04Z-
dc.date.issued2004-
dc.identifier.citationJournal of Virology, 2004, p. 7165-7174, Vol. 78, No. 13en_US
dc.identifier.isbn1098-5514 (online)-
dc.identifier.issn0022-538X (print)-
dc.identifier.urihttp://hdl.handle.net/10261/8390-
dc.description.abstractModulation of the activity of tumor suppressor p53 is a key event in the replication of many viruses. We have studied the function of p53 in African swine fever virus (ASFV) infection by determining the expression and activity of this transcription factor in infected cells. p53 levels are increased at early times of infection and are maintained throughout the infectious cycle. The protein is transcriptionally active, stabilized by phosphorylation, and localized in the nucleus. p53 induces the expression of p21 and Mdm2. Strikingly, these two proteins are located at the cytoplasmic virus factories. The retention of Mdm2 at the factory may represent a viral mechanism to prevent p53 inactivation by the protein. The expression of apoptotic proteins, such as Bax or active caspase-3, is also increased following ASFV infection, although the increase in caspase-3 does not appear to be, at least exclusively, p53 dependent. Bax probably plays a role in the induction of apoptosis in the infected cells, as suggested by the release of cytochrome c from the mitochondria. The significance of p21 induction and localization is discussed in relation to the shutoff of cellular DNA synthesis that is observed in ASFV-infected cells.en_US
dc.description.sponsorshipThis work was supported by grants from the Ministerio de Ciencia y Tecnología (BMC2000-1485 and AGL2002-10220-E) and the European Commission (QLRT-2000-02216) and by an institutional grant from the Fundación Ramón Areces. C. Hurtado was a fellow of Fundación Ramón Arecesen_US
dc.format.extent4159793 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.rightsopenAccessen_US
dc.subjectAfrican swine fever virusen_US
dc.titleModulation of p53 cellular function and cell death by African Swine Fever Virusen_US
dc.typeartículoen_US
dc.identifier.doi10.1128/JVI.78.13.7165-7174.2004-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1128/JVI.78.13.7165-7174.2004en_US
dc.contributor.funderMinisterio de Ciencia y Tecnología (España)-
dc.contributor.funderEuropean Commission-
dc.contributor.funderFundación Ramón Areces-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100006280es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100008054es_ES
dc.identifier.pmid15194793-
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