Journal
FEBS LETTERS
Volume 478, Issue 1-2, Pages 67-71Publisher
WILEY
DOI: 10.1016/S0014-5793(00)01800-7
Keywords
XRCC4; DNA-dependent protein kinase; ataxia-telangiectasia mutated; DNA double-strand break repair; caspase; apoptosis
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We report the p35 and p60 forms of XRCC4 protein, appearing in human leukemia MOLT-4 or U937 cells following X-irradiation or hyperthermia. p35 appeared in conjunction with the cleavage of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and the fragmentation of internucleosomal DNA, and was suppressed by Ac-DEVD-CHO, p35 was also produced in vitro by treating MOLT-4 cell lysate with recombinant caspases, suggesting that p35 was a caspase-cleaved fragment of XRCC4 in apoptotic cell death. p60 was sensitive to treatment with phosphatase or wortmannin and was undetectable in M059J cells deficient in DNA-PKcs. However, p60 was found in ataxia-telangiectasia cells after irradiation. These results indicated p60 as a phosphorylated form of XRCC4, requiring DNA-PKcs but not ataxia-telangiectasia mutated (ATM). (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
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