@misc{oai:repo.qst.go.jp:00067424,
 author = {Mori, Masahiko and Itsukaichi, Hiromi and Kanda, Reiko and Nakamura, Atsuko and Shiomi, Naoko and Aizawa, Shirou and Shiomi, Tadahiro and 森 雅彦 and 五日市 ひろみ and 神田 玲子 and 中村 篤子 and 塩見 尚子 and 相澤 志郎 and 塩見 忠博},
 month = {Aug},
 note = {Ionizing radiation produces a variety of lesions in DNA including single-strand breaks, double strand breaks and base damage. The repair of DNA double-strand breaks in essential for the maintenance of genomic integrity. Failure to repair DNA double-strand breaks result in loss of genetic information, chromosome translocations, carcinogenesis and cell death. XRCC4 is a member of non-homologous end-joining proteins that functioned in DNA double-strand break repair in eukaryote including human. XRCC4 is a DNA ligase IV accessory factor and required for the rejoining of DNA double- strand breaks. Both XRCC4 and DNA ligase IV deficient mice have been generated. Both deficient mice are not viable because of neuronal degeneration caused by p53-induced apoptosis. Cells obtained from XRCC4 or DNA ligase IV deficient embryo are viable, but show reduced cell proliferation and hypersensitivity to ionizing radiation. To study the role of XRCC4 in human cells, we tried to inactivate XRCC4 gene by using gene targeting technology in human colon cancer cell line, HCT116. We have succeeded to disrupt both alleles of XRCC4 gene. Heterozygous (XRCC4+/-)cells showed reduced cell proliferation but normal X Ray-sensitivity, indicating haploinsufficiency in cell proliferation but not in X ray-sensitivity. Homozygous (XRCC4-/-) cells show reduced cell proliferation and increased chromosome aberrations, and are highly sensitive to X-rays., 12th International Congress of Radiation Research},
 title = {Studies on a role of XRCC4 in human cells},
 year = {2003}
}