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Titolo:
Role of the p53-homologue p73 in EZF1-induced apoptosis
Autore:
Stiewe, T; Putzer, BM;
Indirizzi:
Univ Essen Gesamthsch, Sch Med, Inst Mol Biol Canc Res, Essen, Germany Univ Essen Gesamthsch Essen Germany t Mol Biol Canc Res, Essen, Germany
Titolo Testata:
NATURE GENETICS
fascicolo: 4, volume: 26, anno: 2000,
pagine: 464 - 469
SICI:
1061-4036(200012)26:4<464:ROTPPI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-SUPPRESSOR; FLOW-CYTOMETRY; P53; PROTEIN; GENE; NEUROBLASTOMA; EXPRESSION; BINDING; TARGET; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Putzer, BM Univ Essen Gesamthsch, Sch Med, Inst Mol Biol Canc Res, Essen, Germany Univ Essen Gesamthsch Essen Germany Canc Res, Essen, Germany
Citazione:
T. Stiewe e B.M. Putzer, "Role of the p53-homologue p73 in EZF1-induced apoptosis", NAT GENET, 26(4), 2000, pp. 464-469

Abstract

Most human cancers harbour aberrations of cell-cycle control(1), which result in deregulated activity of the E2F transcription factors with concomitant enhanced cell-cycle progression(2). Oncogenic signalling by E2F1 has recently been linked to stabilization and activation of the tumour suppressor p53 (refs 1,3,4). The p73 protein shares substantial sequence homology and functional similarity with p53 (refs 5-7). Hence, several previously considered p53-independent cellular activities may be attributable to p73. Here we provide evidence that E2F1 directly activates transcription of TP73, leading to activation of p53-responsive target genes and apoptosis. Disruption of p73 function by a tumour-derived p53 mutant reduced E2F1-mediated apoptosis. Thus, p73 activation by deregulated E2F1 activity might constitute a p53-independent, anti-tumorigenic safeguard mechanism.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 02:38:21