@prefix pubblicazioni: . @prefix unitaDiPersonaleInterno: . @prefix prodotto: . unitaDiPersonaleInterno:MATRICOLA39385 pubblicazioni:autoreCNRDi prodotto:ID4601 . unitaDiPersonaleInterno:MATRICOLA6655 pubblicazioni:autoreCNRDi prodotto:ID4601 . @prefix prodottidellaricerca: . @prefix istituto: . istituto:CDS059 prodottidellaricerca:prodotto prodotto:ID4601 . @prefix modulo: . modulo:ID2572 prodottidellaricerca:prodotto prodotto:ID4601 . @prefix rdf: . @prefix retescientifica: . prodotto:ID4601 rdf:type retescientifica:ProdottoDellaRicerca , prodotto:TIPO1101 . @prefix rdfs: . prodotto:ID4601 rdfs:label "Identification of an aberrantly spliced form of HDMX in human tumors: a new mechanism for HDM2 stabilization. (Articolo in rivista)"@en . @prefix xsd: . prodotto:ID4601 pubblicazioni:anno "2005-01-01T00:00:00+01:00"^^xsd:gYear ; pubblicazioni:doi "10.1158/0008-5472.CAN-05-0450"^^xsd:string . @prefix skos: . prodotto:ID4601 skos:altLabel "
Giglio S.1, Mancini F.2, Gentiletti F.3, Sparaco G.4, Felicioni L.5, Barassi F.6, Martella C.7, Prodosmo A.8, Iacovelli S.9, Buttitta F.10, Farsetti A.11, Soddu S.12, Marchetti A.13, Sacchi A.14, Pontecorvi A.15, Moretti F.16 (2005)
Identification of an aberrantly spliced form of HDMX in human tumors: a new mechanism for HDM2 stabilization.
in Cancer research (Chic. Ill.)
"^^rdf:HTML ; pubblicazioni:autori "Giglio S.1, Mancini F.2, Gentiletti F.3, Sparaco G.4, Felicioni L.5, Barassi F.6, Martella C.7, Prodosmo A.8, Iacovelli S.9, Buttitta F.10, Farsetti A.11, Soddu S.12, Marchetti A.13, Sacchi A.14, Pontecorvi A.15, Moretti F.16"^^xsd:string ; pubblicazioni:paginaInizio "9687"^^xsd:string ; pubblicazioni:paginaFine "9694"^^xsd:string ; pubblicazioni:altreInformazioni "Impact Factor = 8.649"^^xsd:string ; pubblicazioni:url "http://cancerres.aacrjournals.org/content/65/21/9687.full.pdf+html"^^xsd:string ; pubblicazioni:numeroVolume "65"^^xsd:string . @prefix ns11: . prodotto:ID4601 pubblicazioni:rivista ns11:ID386732 ; pubblicazioni:numeroFascicolo "21"^^xsd:string ; skos:note "ISI Web of Science (WOS)"^^xsd:string , "PubMe"^^xsd:string ; pubblicazioni:affiliazioni "1,2,3,4,8,9,11,12,14,15,16 = Laboratory of Molecular Oncogenesis, Regina Elena Cancer Institute, Rome, Italy;\n11, 16 = Institute of Neurobiology and Molecular Medicine, National Council of Research, Rome, Italy;\n2,15 = Institute of Medical Pathology, Catholic University, Rome, Italy; \n5,6,7,10,13 = Clinical Research Center, Center of Excellence on Aging, University Foundation, Chieti, Italy."^^xsd:string ; pubblicazioni:titolo "Identification of an aberrantly spliced form of HDMX in human tumors: a new mechanism for HDM2 stabilization."^^xsd:string ; prodottidellaricerca:abstract "The HDMX protein is closely related to HDM2 with which it shares different structural domains, particularly the p53 binding domain and the ring finger domain, where the two HDM proteins interact. Several oncogenic forms derived from splicing of HDM2 have been described in cancer. This work aimed at investigating whether analogous forms of HDMX exist in human tumors. Here, we report the characterization of an aberrantly spliced form of HDMX, HDMX211, isolated from the thyroid tumor cell line, ARO. HDMX211 binds and stabilizes the HDM2 protein. Although it lacks the p53 binding domain, HDMX211 also stabilizes p53 by counteracting its degradation by HDM2. However, the resulting p53 is transcriptionally inactive and increasingly associated to its inhibitor HDM2. Expression of HDMX211 strongly enhances the colony-forming ability of human cells in the presence or absence of wild-type p53. Conversely, depletion of HDMX211 by small interfering RNA significantly reduces the growth of ARO cells and increases their sensitivity to chemotherapy. Screening of lung cancer biopsies shows the presence of HDMX211 in samples that overexpress HDM2 protein, supporting a pathologic role for this new protein. This is the first evidence of a variant form of HDMX that has oncogenic potential independently of p53. HDMX211 reveals a new mechanism for overexpression of the oncoprotein HDM2. Most interestingly, it outlines a possible molecular explanation for a yet unclarified tumor phenotype, characterized by simultaneous overexpression of HDM2 and wild-type p53."@en ; prodottidellaricerca:prodottoDi modulo:ID2572 , istituto:CDS059 ; pubblicazioni:autoreCNR unitaDiPersonaleInterno:MATRICOLA6655 , unitaDiPersonaleInterno:MATRICOLA39385 . ns11:ID386732 pubblicazioni:rivistaDi prodotto:ID4601 .