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Titolo:
The human papillomavirus (HPV) 16 E2 protein induces apoptosis in the absence of other HPV proteins and via a p59-dependent pathway
Autore:
Webster, K; Parish, J; Pandya, M; Stern, PL; Clarke, AR; Gaston, K;
Indirizzi:
Univ Bristol, Sch Med Sci, Dept Biochem, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD Bristol BS8 1TD, Avon, England Christie Hosp NHS Trust, Paterson Inst Canc Res, Manchester M20 9BX, Lancs, England Christie Hosp NHS Trust Manchester Lancs England M20 9BX , Lancs, England
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 1, volume: 275, anno: 2000,
pagine: 87 - 94
SICI:
0021-9258(20000107)275:1<87:THP(1E>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARCINOMA CELL-LINES; ONCOGENIC HUMAN PAPILLOMAVIRUSES; TUMOR-SUPPRESSOR PROTEIN; E7 PROTEIN; MEDIATES ASSOCIATION; HUMAN KERATINOCYTES; E6 ONCOPROTEIN; DNA-BINDING; P53; TYPE-16;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Gaston, K Univ Bristol, Sch Med Sci, Dept Biochem, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD S8 1TD, Avon, England
Citazione:
K. Webster et al., "The human papillomavirus (HPV) 16 E2 protein induces apoptosis in the absence of other HPV proteins and via a p59-dependent pathway", J BIOL CHEM, 275(1), 2000, pp. 87-94

Abstract

The human papillomavirus (HPV) E2 protein regulates viral gene expression and is also required for viral replication. HPV-transformed cells often contain chromosomally integrated copies of the HPV genome in which the viral E2 gene is disrupted. We have shown previously that re-expression of the HPV16 E2 protein in HPV 16-transformed cells results in cell death via apoptosis. Here we show that the HPV 16 E2 protein can induce apoptosis in both HPV-transformed and non-HPV-transformed cell lines. E2-induced apoptosis is abrogated by a trans-dominant negative mutant of p53 or by overexpression of the HPV 16 E6 protein, but is increased by overexpression of wild-type p53. We show that mutations that block the DNA binding activity of E2 do not impair the ability of this protein to induce apoptosis. In contrast, removal of both N-terminal domains from the E2 dimer completely blocks E2-inducedcell death. Heterodimers formed between wild-type E2 and N-terminally deleted E2 proteins also fail to induce cell death. Our data suggest that neither the DNA binding activity of E2 nor other HPV proteins are required for the induction of apoptosis by E2 and that E2-induced cell death occurs via ap53-dependent pathway.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 18:18:50