Cleavage and phosphorylation of XRCC4 protein induced by X‐irradiation

FEBS Letters

Ma, Xue-Jun²  Matsumoto, Yoshihisa²  Serizawa, Shinobu²  Tomita, Masanori²  Enomoto, Atsushi²  Suzuki, Norio²  Yasuda, Hideyo¹  Hosoi, Yoshio²  Namba, Naoki²  Hirano, Kazuya²  Sakai, Kazuo²  Morita, Akinori²  Umeda, Noriko² 

[1] School of Life Science, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan;Department of Radiation Oncology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan

关键词: XRCC4;    DNA-dependent protein kinase;    Ataxia-telangiectasia mutated;    DNA double-strand break repair;    Caspase;    Apoptosis;   

DOI  :  10.1016/S0014-5793(00)01800-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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).

【 授权许可】

Unknown