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Titolo:
Papillomavirus E2 induces senescence in HPV-positive cells via pRB- and p21(CIP)-dependent pathways
Autore:
Wells, SI; Francis, DA; Karpova, AY; Dowhanick, JJ; End, JDB; Benson, JD; Howley, PM;
Indirizzi:
Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 h Med, Dept Pathol, Boston, MA 02115 USA
Titolo Testata:
EMBO JOURNAL
fascicolo: 21, volume: 19, anno: 2000,
pagine: 5762 - 5771
SICI:
0261-4189(20001101)19:21<5762:PEISIH>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
RETINOBLASTOMA GENE-PRODUCT; CERVICAL-CARCINOMA CELLS; ADENOVIRUS E1A PROTEINS; TRANSCRIPTIONAL ACTIVATION; REPLICATIVE SENESCENCE; MOLECULAR-CLONING; HUMAN FIBROBLASTS; EPITHELIAL-CELLS; DNA-REPLICATION; E6 PROMOTER;
Keywords:
E2; p21(CIP); papillomavirus; pRB; senescence;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Howley, PM Harvard Univ, Sch Med, Dept Pathol, 200 Longwood Ave, Boston, MA 02115 USA Harvard Univ 200 Longwood Ave Boston MA USA 02115 MA 02115 USA
Citazione:
S.I. Wells et al., "Papillomavirus E2 induces senescence in HPV-positive cells via pRB- and p21(CIP)-dependent pathways", EMBO J, 19(21), 2000, pp. 5762-5771

Abstract

A hallmark of human papillomavirus (HPV) associated carcinogenesis is the integration of the viral DNA into the cellular genome, usually accompanied by the loss of expression of the viral E2 gene. E2 binds to and represses the viral promoter directing expression of the E6 and E7 oncogenes. The re-introduction and expression of exogenous E2 in HPV-positive cancer cells results in cellular growth arrest, while growth in the context of exogenous E2can be restored through the expression of exogenous E6 and E7, Here we examine the individual contributions of the viral E6 and E7 genes to this phenotype, E6 alone displays moderate activity, whereas both E7 and adenovirus E1A display high activity in reversing E2-mediated cellular growth suppression. Using defined mutants of E7 and EIA, we show that an intact retinoblastoma interaction domain is required for this function. In addition, we showthat the E2-mediated growth arrest of HPV-positive cells results in cellular senescence, and implicate the cyclin/cdk inhibitor p21(CIP) as a downstream E2 effector in this phenotype.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 08:28:49