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Titolo:
Regulation of the G2/M transition by p53
Autore:
Taylor, WR; Stark, GR;
Indirizzi:
Cleveland Clin Fdn, Lerner Res Inst, Dept Mol Biol, Cleveland, OH 44195 USA Cleveland Clin Fdn Cleveland OH USA 44195 l Biol, Cleveland, OH 44195 USA
Titolo Testata:
ONCOGENE
fascicolo: 15, volume: 20, anno: 2001,
pagine: 1803 - 1815
SICI:
0950-9232(20010405)20:15<1803:ROTGTB>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA-DAMAGE CHECKPOINT; CELL-CYCLE ARREST; LARGE T-ANTIGEN; PAPILLOMAVIRUS E6 ONCOPROTEINS; TUMOR-SUPPRESSOR PROTEIN; G(2) CHECKPOINT; ATAXIA-TELANGIECTASIA; TRANSCRIPTION FACTOR; BINDING-PROTEIN; KINASE-ACTIVITY;
Keywords:
cell cycle; checkpoint; Cdc2; cyclin; p21; DNA damage;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
126
Recensione:
Indirizzi per estratti:
Indirizzo: Taylor, WR Cleveland Clin Fdn, Lerner Res Inst, Dept Mol Biol, 9500 EuclidAve, Cleveland, OH 44195 USA Cleveland Clin Fdn 9500 Euclid Ave Cleveland OH USA 44195 5 USA
Citazione:
W.R. Taylor e G.R. Stark, "Regulation of the G2/M transition by p53", ONCOGENE, 20(15), 2001, pp. 1803-1815

Abstract

p53 protects mammals from neoplasia by inducing apoptosis, DNA repair and cell cycle arrest in response to a variety of stresses. p53-dependent arrest of cells in the G1 phase of the cell cycle is an important component of the cellular response to stress. Here we review recent evidence that implicates p53 in controlling entry into mitosis when cells enter G2 with damaged DNA or when they are arrested in S phase due to depletion of the substratesrequired for DNA synthesis, Part of the mechanism by which p53 blocks cells at the G2 checkpoint involves inhibition of Cdc2, the cyclin-dependent kinase required to enter mitosis. Cdc2 is inhibited simultaneously by three transcriptional targets of p53, Gadd45, p21, and 14-3-3 sigma. Binding of Cdc2 to Cyclin B1 is required for its activity, and repression of the cyclin BI gene by p53 also contributes to blocking entry into mitosis, p53 also represses the cdc2 gene, to help ensure that cells do not escape the initial block. Genotoxic stress also activates p53-independent pathways that inhibit Cdc2 activity, activation of the protein kinases Chk1 and Chk2 by the protein kinases Atm and Atr, Chk1 and Chk2 inhibit Cdc2 by inactivating Cdc25,the phosphatase that normally activates Cdc2. Chk1, Chk2, Atm and Atr alsocontribute to the activation of p53 in response to genotoxic stress and therefore play multiple roles, p53 induces transcription of the reprimo, B99,and mcg10 genes, all of which contribute to the arrest of cells in G2, butthe mechanisms of cell cycle arrest by these genes is not known. Repression of the topoisomer ase II gene by p53 helps to block entry into mitosis and strengthens the G2 arrest. In summary, multiple overlapping p53-dependentand p53-independent pathways regulate the G2/M transition in response to genotoxic stress.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 06:47:41