p53 status, DNA double-strand break repair proficiency, and radiation response of mouse lymphoid and myeloid cell lines.
The p53 status of a panel of 10 mouse lymphoid or myeloid cell lines was determined by immunoprecipitation with mutant- and wild-type-specific antibodies and was compared with the radiation response of the lines. The more rapidly dying cell lines all contained p53 displaying the wild-type epitope. By contrast, four of six more slowly dying cell lines contained either no or mutant p53 protein. It was of interest that radiation-induced apoptosis occurred, albeit at a considerable time after irradiation, in cells ostensibly lacking p53 protein. DNA double-strand break (dsb) repair was examined in both a rapidly and more slowly dying cell line. The rapidly dying cell line was capable of DNA dsb rejoining, however this repair was interrupted by postirradiation DNA degradation.
Radford
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Research Division, Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia.
D000818:Animals; D002460:Cell Line; D004247:DNA / Q000528:radiation effects*; D004249:DNA Damage; D004260:DNA Repair; D051379:Mice; D011836:Radiation Tolerance; D016159:Tumor Suppressor Protein p53 / Q000032:analysis*
D016159:Tumor Suppressor Protein p53; D004247:DNA