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Titolo:
TRANSCRIPTIONAL ACTIVATION BY P53, BUT NOT INDUCTION OF THE P21 GENE,IS ESSENTIAL FOR ONCOGENE-MEDIATED APOPTOSIS
Autore:
ATTARDI LD; LOWE SW; BRUGAROLAS J; JACKS T;
Indirizzi:
MIT,CTR CANC RES CAMBRIDGE MA 02139 MIT,CTR CANC RES CAMBRIDGE MA 02139 MIT,HOWARD HUGHES MED INST CAMBRIDGE MA 02139 MIT,DEPT BIOL CAMBRIDGE MA 02139 COLD SPRING HARBOR LABS COLD SPRING HARBOR NY 11724
Titolo Testata:
EMBO journal
fascicolo: 14, volume: 15, anno: 1996,
pagine: 3693 - 3701
SICI:
0261-4189(1996)15:14<3693:TABPBN>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
WILD-TYPE P53; CELL-CYCLE ARREST; P53-DEPENDENT APOPTOSIS; CANCER-THERAPY; IN-VIVO; PROTEIN; MICE; SUPPRESSION; INHIBITOR; SPECTRUM;
Keywords:
APOPTOSIS; G(1) ARREST; P53; P21; TRANSCRIPTIONAL TRANSACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
L.D. Attardi et al., "TRANSCRIPTIONAL ACTIVATION BY P53, BUT NOT INDUCTION OF THE P21 GENE,IS ESSENTIAL FOR ONCOGENE-MEDIATED APOPTOSIS", EMBO journal, 15(14), 1996, pp. 3693-3701

Abstract

The p53 tumor suppressor limits cellular proliferation by inducing either G(1) arrest or apoptosis, depending on the cellular context, To determine if these pathways are mechanistically distinct, we have examined the effects of different p53 mutants in p53 null primary mouse embryo fibroblasts. We chose this system as it is highly physiological and ensures that the interpretation of the results will not be confounded by the presence of endogenous p53 or oncoproteins which target p53, Using single cell microinjection assays for both G(1) arrest and apoptosis, with loss-of-function and chimeric gain-of-function mutants, we have demonstrated that transcriptional activation is critical for bothprocesses, Replacement of the p53 activation domain with that of VP16, or replacement of the p53 oligomerization domain with that of GCN4, reconstituted both G(1) arrest and apoptosis activities, However, despite the importance of transcriptional activation in both processes, the target gene requirements are different, The p21 cyclin-dependent kinase inhibitor, which has been shown to be a direct target of p53 and acomponent of the radiation-induced G(1) arrest response, is dispensable for oncogene-induced apoptosis, suggesting that these two p53-dependent transcriptional pathways are distinct.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 19:51:46