@article{oai:repo.qst.go.jp:00045365,
 author = {Uehara, Yosihiko and Ikehata, Hironobu and Hirayama, Ryoichi and Furusawa, Yoshiya and Ando, Koichi and Ono, Tetsuya and et.al and 上原 芳彦 and 平山 亮一 and 古澤 佳也 and 安藤 興一},
 issue = {2},
 journal = {Radiation Research},
 month = {Aug},
 note = {With the goal of understanding the role of non-homologous end-joining repair in the maintenance of genetic information at the tissue level, we studied mutations induced by radiation and subsequent repair of DNA double-strand breaks in Ku70 gene-deficient lacZ transgenic mice. The local mutation frequencies and types of mutations were analyzed on a lacZ gene that had been chromosomally integrated, which allowed us to monitor DNA sequence alterations within this 3.1-kbp region. The mutagenic process leading to the development of the most frequently observed small deletions in wild-type mice after exposure to 20 Gy of X rays was suppressed in Ku70 mice in the three tissues examined: spleen, liver and brain. Examination of DNA break rejoining and the phosphorylation of histone H2AX in Ku70-deficient and -proficient mice revealed that Ku70 deficiency decreased the frequency of DNA rejoining, suggesting that DNA rejoining is one of the causes of radiation-induced deletion mutations. Limited but statistically significant DNA rejoining was found in the liver and brain of Ku70-deficient mice 3.5 days after irradiation, showing the presence of a DNA double-strand break repair system other than non-homologous end joining. These data indicate a predominant role of non-homologous end joining in the production of radiation-induced mutations in vivo.},
 pages = {216--223},
 title = {Absence of Ku70 Gene Obliterates X-Ray-Induced lacZ Mutagenesis of Small Deletions in Mouse Tissues},
 volume = {170},
 year = {2008}
}