Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation

Yoshihisa Matsumoto; Norio Suzuki; Naoki Namba; Noriko Umeda; Xue Jun Ma; Akinori Morita; Masanori Tomita; Atsushi Enomoto; Shinobu Serizawa; Kazuya Hirano; Kazuo Sakai; Hideyo Yasuda; Yoshio Hosoi

doi:10.1016/S0014-5793(00)01800-7

Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation

Yoshihisa Matsumoto, Norio Suzuki, Naoki Namba, Noriko Umeda, Xue Jun Ma, Akinori Morita, Masanori Tomita, Atsushi Enomoto, Shinobu Serizawa, Kazuya Hirano, Kazuo Sakai, Hideyo Yasuda, Yoshio Hosoi

MED - Medical Sciences

Research output: Contribution to journal › Article › peer-review

56 Citations (Scopus)

Abstract

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). Copyright (C) 2000 Federation of European Biochemical Societies.

Original language	English
Pages (from-to)	67-71
Number of pages	5
Journal	FEBS Letters
Volume	478
Issue number	1-2
DOIs	https://doi.org/10.1016/S0014-5793(00)01800-7
Publication status	Published - 2000 Jul 28

Keywords

Apoptosis
Ataxia-telangiectasia mutated
Caspase
DNA double-strand break repair
DNA-dependent protein kinase
XRCC4

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10.1016/S0014-5793(00)01800-7

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@article{1e391ea10d954feeaa3f9bed948f6d56,

title = "Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation",

abstract = "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). Copyright (C) 2000 Federation of European Biochemical Societies.",

keywords = "Apoptosis, Ataxia-telangiectasia mutated, Caspase, DNA double-strand break repair, DNA-dependent protein kinase, XRCC4",

author = "Yoshihisa Matsumoto and Norio Suzuki and Naoki Namba and Noriko Umeda and Ma, {Xue Jun} and Akinori Morita and Masanori Tomita and Atsushi Enomoto and Shinobu Serizawa and Kazuya Hirano and Kazuo Sakai and Hideyo Yasuda and Yoshio Hosoi",

note = "Funding Information: We thank Dr. Makoto Takeuchi, Dr. Shunsaku Ando and Dr. Masashi Kurimoto at the Fujisaki Institute of Hayashibara Biochemical Laboratories (Okayama, Japan) for the large number of MOLT-4 cells and Dr. Koh-ichi Sakata (Sapporo Medical University) for discussion and encouragement. This study was partly supported by a Grant-in-Aid from the Ministry of Education, Science, Sports and Culture, Ministry of Health and Welfare of Japan and Ground Research for Space Utilization promoted by NASDA and Japan Space Forum.",

year = "2000",

month = jul,

day = "28",

doi = "10.1016/S0014-5793(00)01800-7",

language = "English",

volume = "478",

pages = "67--71",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Wiley-Blackwell",

number = "1-2",

}

TY - JOUR

T1 - Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation

AU - Matsumoto, Yoshihisa

AU - Suzuki, Norio

AU - Namba, Naoki

AU - Umeda, Noriko

AU - Ma, Xue Jun

AU - Morita, Akinori

AU - Tomita, Masanori

AU - Enomoto, Atsushi

AU - Serizawa, Shinobu

AU - Hirano, Kazuya

AU - Sakai, Kazuo

AU - Yasuda, Hideyo

AU - Hosoi, Yoshio

N1 - Funding Information: We thank Dr. Makoto Takeuchi, Dr. Shunsaku Ando and Dr. Masashi Kurimoto at the Fujisaki Institute of Hayashibara Biochemical Laboratories (Okayama, Japan) for the large number of MOLT-4 cells and Dr. Koh-ichi Sakata (Sapporo Medical University) for discussion and encouragement. This study was partly supported by a Grant-in-Aid from the Ministry of Education, Science, Sports and Culture, Ministry of Health and Welfare of Japan and Ground Research for Space Utilization promoted by NASDA and Japan Space Forum.

PY - 2000/7/28

Y1 - 2000/7/28

N2 - 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). Copyright (C) 2000 Federation of European Biochemical Societies.

AB - 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). Copyright (C) 2000 Federation of European Biochemical Societies.

KW - Apoptosis

KW - Ataxia-telangiectasia mutated

KW - Caspase

KW - DNA double-strand break repair

KW - DNA-dependent protein kinase

KW - XRCC4

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U2 - 10.1016/S0014-5793(00)01800-7

DO - 10.1016/S0014-5793(00)01800-7

M3 - Article

C2 - 10922471

AN - SCOPUS:0034726003

SN - 0014-5793

VL - 478

SP - 67

EP - 71

JO - FEBS Letters

JF - FEBS Letters

IS - 1-2

ER -

Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation

Abstract

Keywords

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