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Titolo:
Radiosensitivity in Nijmegen Breakage syndrome cells is attributable to a repair defect and not cell cycle checkpoint defects
Autore:
Girard, PM; Foray, N; Stumm, M; Waugh, A; Riballo, E; Maser, RS; Phillips, WP; Petrini, J; Arlett, CF; Jeggo, PA;
Indirizzi:
Univ Sussex, MRC, Cell Mutat Unit, Brighton BN1 9RR, E Sussex, England Univ Sussex Brighton E Sussex England BN1 9RR BN1 9RR, E Sussex, England Inst Gustave Roussy, CNRS, UMR1599, F-94805 Villejuif, France Inst GustaveRoussy Villejuif France F-94805 , F-94805 Villejuif, France Univ Magdeburg Klinikum, Inst Humangenet, D-39120 Magdeburg, Germany Univ Magdeburg Klinikum Magdeburg Germany D-39120 120 Magdeburg, Germany Univ Wisconsin, Dept Expt Therapy, Genet Lab, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 apy, Genet Lab, Madison, WI 53706 USA Royal Free Hosp, London NW3 2PF, England Royal Free Hosp London England NW3 2PF ree Hosp, London NW3 2PF, England
Titolo Testata:
CANCER RESEARCH
fascicolo: 17, volume: 60, anno: 2000,
pagine: 4881 - 4888
SICI:
0008-5472(20000901)60:17<4881:RINBSC>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
DOUBLE-STRAND BREAKS; CHROMOSOMAL INSTABILITY DISORDER; DNA-DAMAGE RESPONSE; END-JOINING REPAIR; ATAXIA-TELANGIECTASIA; SACCHAROMYCES-CEREVISIAE; IONIZING-RADIATION; HUMAN FIBROBLASTS; PROTEIN COMPLEX; ATM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Jeggo, PA Univ Sussex, MRC, Cell Mutat Unit, Brighton BN1 9RR, E Sussex, England Univ Sussex Brighton E Sussex England BN1 9RR E Sussex, England
Citazione:
P.M. Girard et al., "Radiosensitivity in Nijmegen Breakage syndrome cells is attributable to a repair defect and not cell cycle checkpoint defects", CANCER RES, 60(17), 2000, pp. 4881-4888

Abstract

Cells derived from Nijmegen Breakage Syndrome (NBS) patients display radiosensitivity and cell cycle checkpoint defects. Here, we examine whether theradiosensitivity of NBS cells is the result of a repair defect or whether it can be attributed to impaired checkpoint arrest, We report a small increased fraction of unrejoined double strand breaks and, more significantly, increased chromosome breaks in noncycling NBS cells at 24 h after irradiation. One of the NBS lines examined (347BR) was atypical in showing a nearly normal checkpoint response. In contrast to the mild checkpoint defect, 347BRdisplays marked gamma-ray sensitivity similar to that shown by other NBS lines. Thus, the gamma-ray sensitivity correlates with the repair defect rather than impaired checkpoint control. Taken together, the results provide direct evidence for a repair defect in NBS cells and are inconsistent with the suggestion that the radiosensitivity is attributable only to impaired checkpoint arrest. 347BR also displays elevated spontaneous damage that cannot be attributed to impaired G(2)-M arrest, suggesting a function of Nbs1 indecreasing or limiting the impact of spontaneously arising double strand breaks.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:30:59