@prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . @prefix prodotto: . unitaDiPersonaleInterno:MATRICOLA9453 pubblicazioni:autoreCNRDi prodotto:ID11309 . @prefix prodottidellaricerca: . @prefix istituto: . istituto:CDS013 prodottidellaricerca:prodotto prodotto:ID11309 . unitaDiPersonaleInterno:MATRICOLA12051 pubblicazioni:autoreCNRDi prodotto:ID11309 . @prefix rdf: . @prefix retescientifica: . prodotto:ID11309 rdf:type retescientifica:ProdottoDellaRicerca , prodotto:TIPO1101 . @prefix rdfs: . prodotto:ID11309 rdfs:label "E1A deregulates the centrosome cycle in a Ran GTPase-dependent manner. (Articolo in rivista)"@en . @prefix xsd: . prodotto:ID11309 pubblicazioni:anno "2003-01-01T00:00:00+01:00"^^xsd:gYear . @prefix skos: . prodotto:ID11309 skos:altLabel "
De Luca A, Mangiacasale R, Severino A, Malquori L, Baldi A, Palena A, Mileo AM, Lavia P, Paggi MG. (2003)
E1A deregulates the centrosome cycle in a Ran GTPase-dependent manner.
in Cancer research (Chic. Ill.)
"^^rdf:HTML ; pubblicazioni:autori "De Luca A, Mangiacasale R, Severino A, Malquori L, Baldi A, Palena A, Mileo AM, Lavia P, Paggi MG."^^xsd:string ; pubblicazioni:paginaInizio "1430"^^xsd:string ; pubblicazioni:paginaFine "1437"^^xsd:string ; pubblicazioni:altreInformazioni "The induction of genomic instability in viral carcinogenesis has now been recognized for almost twenty years. The findings in this paper provide a novel mechanism and expand our understanding of viral oncogenesis. These results were obtained in the framework of a very fruitful collaboration between our lab and colleagues at the Regina Elena Cancer Institute in Rome (both first authorship and senior authorship are joint in this publication). The paper is published in a prestigious journal published by the American Association for Cancer Research with an impact factor of 8,3 in 2002."^^xsd:string ; pubblicazioni:numeroVolume "63"^^xsd:string . @prefix ns10: . prodotto:ID11309 pubblicazioni:rivista ns10:ID386732 ; pubblicazioni:descrizioneSinteticaDelProdotto "This paper shows that small DNA tumor viruses (such as Adenovirus, papilloma virus and SV40) encode proteins that can interact physically and functionally with the GTPase Ran, a major regulator of cell biology and a crucial player in control of the mitotic division Indeed, we show that wild-type oncoproteins that do interact with Ran induce mitotic abnormalities and genomic instability in host cells; in contrast, deleted oncoproteins that cannot interact with Ran have no mitotic effect, although other oncogenic functions are conserved. This is an important finding, in that it may provide the molecular basis for the detrimental effects produced by these oncoproteins in the genome of infected cells."^^xsd:string ; skos:note "ISI Web of Science (WOS)"^^xsd:string ; pubblicazioni:affiliazioni "Istituto Regina Elena per lo Studio e la Cura dei Tumori, Roma; Istituto di Biologia e Patologia Molecolari CNR, Roma."^^xsd:string ; pubblicazioni:titolo "E1A deregulates the centrosome cycle in a Ran GTPase-dependent manner."^^xsd:string ; prodottidellaricerca:abstract "By means of the yeast two-hybrid system, we have discovered a novel physical interaction between the adenovirus E1A oncoprotein and Ran, a small GTPase which regulates nucleocytoplasmic transport, cell cycle progression, and mitotic spindle organization. Expression of E1A elicits induction of S phase and centrosome amplification in a variety of rodent cell lines. The induction of supernumerary centrosomes requires functional RCC1, the nucleotide exchange factor for Ran and, hence, a functional Ran network. The E1A portion responsible for the interaction with Ran is the extreme NH(2)-terminal region (amino acids 1-36), which is also required for the induction of centrosome amplification. In an in vitro assay with recombinant proteins, wild-type E1A interferes with nucleotide exchange on Ran, whereas an E1A mutant, deleted from the extreme NH(2)-terminal region, does not. In addition, we detected an in vitro interaction between Ran and HPV-16 E7 and SV40 large T antigen, two oncoproteins functionally related to E1A. These findings suggest a common pathway of these oncoproteins in eliciting virus-induced genomic instability." ; prodottidellaricerca:prodottoDi istituto:CDS013 ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA12051 , unitaDiPersonaleInterno:MATRICOLA9453 . @prefix parolechiave: . prodotto:ID11309 parolechiave:insiemeDiParoleChiave . ns10:ID386732 pubblicazioni:rivistaDi prodotto:ID11309 . parolechiave:insiemeDiParoleChiaveDi prodotto:ID11309 .