@prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . @prefix prodotto: . unitaDiPersonaleInterno:MATRICOLA5768 pubblicazioni:autoreCNRDi prodotto:ID259783 . @prefix rdf: . @prefix retescientifica: . prodotto:ID259783 rdf:type retescientifica:ProdottoDellaRicerca , prodotto:TIPO1302 . @prefix rdfs: . prodotto:ID259783 rdfs:label "Cell cycle arrest by human cytomegalovirus 86-kDa IE2 protein resembles premature senescence. XII International Congress of Virology (Parigi 27.07-01.08.2002). (Abstract/Poster in atti di convegno)"@en . @prefix xsd: . prodotto:ID259783 pubblicazioni:anno "2002-01-01T00:00:00+01:00"^^xsd:gYear . @prefix skos: . prodotto:ID259783 skos:altLabel "
Noris E., Zannetti C., Sinclair J., Gariglio M., and Landolfo S. (2002)
Cell cycle arrest by human cytomegalovirus 86-kDa IE2 protein resembles premature senescence. XII International Congress of Virology (Parigi 27.07-01.08.2002).
in XII International Congress of Virology, Paris, France, 27.07-01.08.2002
"^^rdf:HTML ; pubblicazioni:autori "Noris E., Zannetti C., Sinclair J., Gariglio M., and Landolfo S."^^xsd:string ; skos:note "Poster"^^xsd:string ; pubblicazioni:affiliazioni "NE: IVV CNR\nZC, LS, GM: Department of Public Health and Microbiology, University of Torino, Via Santena 9, 10100 Torino, Italy\nSJ: Department of Medicine, University of Cambridge, Cambridge CB2 2QQ, UK \nGM: Medical School of Novara, University of Eastern Piedmont, Via Solaroli 17, Novara, Italy"^^xsd:string ; pubblicazioni:titolo "Cell cycle arrest by human cytomegalovirus 86-kDa IE2 protein resembles premature senescence. XII International Congress of Virology (Parigi 27.07-01.08.2002)."^^xsd:string . @prefix prodottidellaricerca: . prodotto:ID259783 prodottidellaricerca:abstract "Primary human embryo fibroblasts (HELF) and adulf diploid fibroblasts (HDF) infected by human cytomegalovirus (HCMV) display ?-galactosidase activity at neutral pH (SA-?-gal), and overexpression of the plasminogen activator inhibitor type-1 (PAI-1) gene, two widely recognized markers of premature cell senescence. The activity depends on culture conditions, being higher when cells are serum starved for 48 hours before infection. Fibroblasts infected by HCMV do not incorporate BrdU, a prerequisite for the formal definition of senescence. At the molecular level, cells infected by HCMV, beside the accumulation of high amounts of negative cell cycle regulators p53 and pRb, display a strong induction of the cyclin dependent kinase inhibitor (cdki) p16INK4a, a possible direct effector of the senescent phenotype, while no difference in the cdki p21CIP1 was observed. The induction of SA-?-gal is confined to fibroblasts and is not evident when the human astrocytoma U373 cells are infected. Moreover, in this tumor cell line, HCMV is not able to modulate the levels of neither p53 nor p16INK4a , suggesting that senescence induction may depend on the integrity of these widely recognized cell cycle regulators. \nHCMV infection assays carried out in the presence of phosphonomorphic acids, that inhibit the virus polymerase and the expression of downstream viral genes, indicated that immediate early and early genes are sufficient for the induction of SA-?-gal. \nBaculovirus vectors expressing HCMV IE1-72 or IE2-86 were inoculated into fibroblasts. An increase of p16INK4a similar to that observed with the whole virus, together with the induction of SA-?-gal were observed, primarily with IE2-86, suggesting that the viral IE2 gene leads infected cells into a senescent state. Altogether our results demonstrate that HCMV, after arresting the cell cycle and inhibiting the apoptosis, triggers the cellular senescence program likely though the p53 and p16 INK4a pathways."@en ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA5768 .