Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation

被引：55

作者：

Matsumoto, Y

Suzuki, N

Namba, N

Umeda, N

Ma, XJ

Morita, A

Tomita, M

Enomoto, A

Serizawa, S

Hirano, K

Sakai, K

Yasuda, H

Hosoi, Y

机构：

[1] Univ Tokyo, Fac Med, Dept Radiat Oncol, Bunkyo Ku, Tokyo 1130033, Japan

[2] Tokyo Univ Pharm & Life Sci, Sch Life Sci, Tokyo 1920392, Japan

[3] Cent Res Inst Elect Power Ind, Abiko Res Lab, Komae Branch, Dept Biosci, Tokyo 2018511, Japan

来源：

FEBS LETTERS | 2000年 / 478卷 / 1-2期

关键词：

XRCC4; DNA-dependent protein kinase; ataxia-telangiectasia mutated; DNA double-strand break repair; caspase; apoptosis;

D O I：

10.1016/S0014-5793(00)01800-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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). (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：67 / 71

页数：5

共 39 条

[1] Enhanced phosphorylation of p53 by ATN in response to DNA damage [J].