@misc{oai:repo.qst.go.jp:00069018,
 author = {Shiomi, Tadahiro and Shiomi, Naoko and Mori, Masahiko and Tsuji, Hideo and Imai, Takashi and Inoue, Hirokazu and Tateishi, Satoshi and Yamaizumi, Masaru and 塩見 忠博 and 塩見 尚子 and 森 雅彦 and 辻 秀雄 and 今井 高志},
 month = {Jul},
 note = {Proliferating cell nuclear antigen (PCNA) is monoubiquitinated in a RAD18/RAD6-dependent manner at stalled replication forks caused by DNA lesions. PCNA monoubiquitination mediates a polymerase switch from replicative to translesion polymerase to continue replication. Therefore, RAD18-deficient cells become sensitive to various DNA damaging agents. However, PCNA was not monoubiquitinated after X-irradiation in human cell line HCT116, although it's RAD18 deficient mutant was sensitive to X rays and defective in repair of X ray-induced chromosome aberrations.The mutant cells were hypersensitive to topoisomerase I inhibitor camptothecin that generated single strand breaks (SSBs) but not to topoisomerase II inhibitor etoposide that generated double strand breaks. Thus, human RAD18 is required for the repair of chromosomal SSBs and PCNA monoubiquitination is not necessary for the repair process., The 13th International Congress of Radiation Research},
 title = {Human RAD18 is involved in single-strand break repair independent of PCNA monoubiquitination},
 year = {2007}
}