| Autor: |
Ishizaki K; Radiation Biology Center, Kyoto University, Japan., Ejima Y, Matsunaga T, Hara R, Sakamoto A, Ikenaga M, Ikawa Y, Aizawa S |
| Jazyk: |
angličtina |
| Zdroj: |
International journal of cancer [Int J Cancer] 1994 Jul 15; Vol. 58 (2), pp. 254-7. |
| DOI: |
10.1002/ijc.2910580218 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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