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Accumulation of p53 protein was seen in the nuclei of mammalian cells following DNA damage caused by ultraviolet radiation (UV), X-ray, or a restriction enzyme. Promoters containing p53-binding sites show a dramatic transcriptional response to DNA damage. The p53 response to X-ray is rapid, reaching a peak at 2 hr after radiation, but is very transitory and reduced in magnitude compared with that seen in response to UV. We find no substantive defect in the p53 response of cells from ataxia telangiectasia or xeroderma pigmentosum complementation group A patients. In contrast, 2 out of 11 primary cultures from Bloom's patients showed a complete absence of p53 accumulation following UV irradiation or SV40 infection and a grossly delayed and aberrant response following X-ray.

More information Original publication

DOI

10.1016/0092-8674(93)90496-d

Type

Journal article

Publication Date

1993-11-19T00:00:00+00:00

Volume

75

Pages

765 - 778

Total pages

13

Keywords

Apoptosis, Ataxia Telangiectasia, Bloom Syndrome, Cell Cycle, Cell Line, DNA Damage, Dose-Response Relationship, Radiation, Fluorescent Antibody Technique, Gene Expression Regulation, Genes, p53, Heat-Shock Proteins, Humans, In Vitro Techniques, RNA, Messenger, Radiation, Ionizing, Tumor Suppressor Protein p53, Ultraviolet Rays, Xeroderma Pigmentosum