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Publication : Increased UV-induced SCEs but normal repair of DNA damage in p53-deficient mouse cells.

First Author  Ishizaki K Year  1994
Journal  Int J Cancer Volume  58
Issue  2 Pages  254-7
PubMed ID  8026887 Mgi Jnum  J:19174
Mgi Id  MGI:67369 Doi  10.1002/ijc.2910580218
Citation  Ishizaki K, et al. (1994) Increased UV-induced SCEs but normal repair of DNA damage in p53-deficient mouse cells. Int J Cancer 58(2):254-7
abstractText  UV-induced sister chromatid exchanges (SCEs) in p53-deficient mouse cells were studied to obtain more evidence regarding the involvement of p53 protein in the DNA repair pathway as a checkpoint protein. After 5 J/m2 UV irradiation, mutant-type homozygous cells for p53-deficiency showed the same number of SCEs as the heterozygous and wild-type homozygous cells. In the heterozygous and wild-type homozygous cells, no further increase of SCEs was observed after 10 J/m2 UV irradiation. In contrast, in mutant-type homozygous cells about twice as many SCEs were induced by 10 J/m2 UV as by 5 J/m2 UV. In mutant-type homozygous cells, fractions of S-phase cells decreased just after 10 J/m2 UV irradiation, but recovered to higher than control levels within a short time, while in heterozygous and wild-type homozygous cells, the decrease in S-phase cells was prolonged by more than 6 hr and no increase above control levels was observed. Although no difference in UV sensitivity and repair of UV-induced DNA damage was found among the 3 genotypes, which were determined by the relative colony-forming ability after UV irradiation and removal of thymine dimers and (6-4) photoproducts from cellular DNA, our data strongly suggest an impaired checkpoint function in p53-deficient cells when DNA is damaged.
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