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Titolo:
P53 REGULATES CDC2 INDEPENDENTLY OF INHIBITORY PHOSPHORYLATION TO REINFORCE RADIATION-INDUCED G2 ARREST IN HUMAN-CELLS
Autore:
WINTERS ZE; ONGKEKO WM; HARRIS AL; NORBURY CJ;
Indirizzi:
UNIV OXFORD,INST MOL MED,ONCOL MOL LAB,IMPERIAL CANC RES FUND,JOHN RADCLIFFE HOSP OXFORD OX3 9DS ENGLAND UNIV OXFORD,INST MOL MED,ONCOL MOL LAB,IMPERIAL CANC RES FUND,JOHN RADCLIFFE HOSP OXFORD OX3 9DS ENGLAND
Titolo Testata:
Oncogene
fascicolo: 6, volume: 17, anno: 1998,
pagine: 673 - 684
SICI:
0950-9232(1998)17:6<673:PRCIOI>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLIN-DEPENDENT KINASES; P34CDC2 PROTEIN-KINASE; HUMAN CANCER-CELLS; TYROSINE PHOSPHORYLATION; DNA-DAMAGE; CHECKPOINT CONTROL; FISSION YEAST; SACCHAROMYCES-CEREVISIAE; TYR15 PHOSPHORYLATION; G(2) DELAY;
Keywords:
P53; CELL CYCLE; CHECKPOINT; G2; CDC2; PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
Z.E. Winters et al., "P53 REGULATES CDC2 INDEPENDENTLY OF INHIBITORY PHOSPHORYLATION TO REINFORCE RADIATION-INDUCED G2 ARREST IN HUMAN-CELLS", Oncogene, 17(6), 1998, pp. 673-684

Abstract

We have investigated the influence of p53 on radiation-induced G2 cell cycle arrest using human H1299 cells expressing temperature-sensitive p53. Gamma-irradiated cells lacking p53 arrested transiently in G2 with Cdc2 extensively phosphorylated at the inhibitory sites Thr14 and Tyr15, and with both Cdc2 and cyclin B1 restricted to the cytoplasm. Activation of p53 by temperature shift resulted in a more protracted G2arrest that could not be overridden by checkpoint-abrogating drugs. Surprisingly, this enhancement of G2 arrest was associated with a marked lack of inhibitory phosphorylation of Cdc2 and with the nuclear localization of both Cdc2 and cyclin B1. While transient expression of an A14F15 mutant form of Cdc2 that is not subject to inhibitory phosphorylation induced mitotic catastrophe in cells lacking p53, the p53-expressing cells were relatively refractory to this effect. Enforced expression of p21(WAF1/CIP1) was sufficient to confer nuclear localization on Cdc2 in the p53 null cells, though immunodepletion experiments demonstrated that only a small proportion of Cdc2 was stably associated with p21(WAF1/CIP1) in the p53-expressing cells. We conclude that a p53-dependent pathway can operate after exposure of human cells to ionisingradiation to promote G2 arrest accompanied by nuclear translocation rather than inhibitory phosphorylation of Cdc2.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 15:37:45