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Johnson, N.F.; Gurule, D.M.; Carpenter, T.R.
Inhalation Toxicology Research Institute. Annual report, October 1, 1994--September 30, 19951995
Inhalation Toxicology Research Institute. Annual report, October 1, 1994--September 30, 19951995
AbstractAbstract
[en] One role of the p53 tumor suppressor protein has been recently revealed. Kastan, M.B. reported that p53 protein accumulates in cells exposed to ionizing radiation. The accumulation of p53 protein is in response to DNA damage, most importantly double-strand breaks, that results from exposure to ionizing radiation. The rise in cellular p53 levels is necessary for an arrest in the G1 phase of the cell cycle to provide additional time for DNA repair. The p53 response has also been demonstrated to enhance PCNA-dependent repair. p53 is thus an important regulator of the cellular response to DNA-damaging radiation. From this data, it can be concluded that the magnitude of the p53 response is not dependent on the phase of culture growth
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Bice, D.E.; Hahn, F.F.; Hoover, M.D.; Neft, R.E.; Thornton-Manning, J.R.; Bradley, P.L. (eds.); Lovelace Biomedical and Environmental Research Inst., Albuquerque, NM (United States). Inhalation Toxicology Research Inst; 214 p; Dec 1995; p. 110-112; Also available from OSTI as DE96008986; NTIS; US Govt. Printing Office Dep
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