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Titolo:
P53 null mice: damaging the hypothesis?
Autore:
Sansom, OJ; Clarke, AR;
Indirizzi:
Cardiff Univ, Cardiff Sch Business, Cardiff CF10 3US, S Glam, Wales Cardiff Univ Cardiff S Glam Wales CF10 3US ardiff CF10 3US, S Glam, Wales Univ Edinburgh, Sch Med, Dept Pathol, Edinburgh EH8 9AG, Midlothian, Scotland Univ Edinburgh Edinburgh Midlothian Scotland EH8 9AG Midlothian, Scotland
Titolo Testata:
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
fascicolo: 2, volume: 452, anno: 2000,
pagine: 149 - 162
SICI:
1386-1964(20000918)452:2<149:PNMDTH>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOUSE INTESTINAL EPITHELIUM; RADIATION-INDUCED APOPTOSIS; FEMALE EMBRYONIC LETHALITY; BLUE(R) TRANSGENIC MOUSE; MURINE SMALL-INTESTINE; KINASE C-ABL; DNA-DAMAGE; P53-DEFICIENT MICE; MUTATION FREQUENCY; IN-VIVO;
Keywords:
P53; mice; tumour suppressor gene;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
81
Recensione:
Indirizzi per estratti:
Indirizzo: Clarke, AR Cardiff Univ, Cardiff Sch Business, POB 911, Cardiff CF10 3US, S Glam, Wales Cardiff Univ POB 911 Cardiff S Glam Wales CF10 3US Glam, Wales
Citazione:
O.J. Sansom e A.R. Clarke, "P53 null mice: damaging the hypothesis?", MUT RES-F M, 452(2), 2000, pp. 149-162

Abstract

P53 is extremely well characterised as a tumour suppressor gene, and many activities have been attributed to it which are consistent with this function. However, despite being the subject of intense study it still remains unclear precisely which of these functions is crucial to its in vivo role as a tumour suppressor gene. This is particularly true of its role in the induction of apoptosis. The original observation of p53-dependent apoptosis gave rise to the following hypothesis: namely, that p53 deficiency leads to a persistence of DNA damaged cells which are the potential founders of malignancy. This review summarises the data for and against this hypothesis, withspecific emphasis on data obtained from studies of the murine intestine. What emerges from these studies is a complex picture, where data can be obtained in support of this hypothesis, but there are many circumstances which exist where it is not supported. Taken together this collection of data suggests that the abrogation of p53-dependent apoptosis may indeed impact uponcarcinogenesis and neoplastic progression, but that the simplistic notion of p53 as the single gatekeeper of this pathway is untenable. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 17:14:03