@article{oai:repo.qst.go.jp:00044807,
 author = {Noguchi, Miho and Yu, Dong and Hirayama, Ryoichi and Ninomiya, Yasuharu and Sekine, Emiko and Kubota, Nobuo and Ando, Koichi and Okayasu, Ryuichi and 野口 実穂 and 于 冬 and 平山 亮一 and 二宮 康晴 and 関根 絵美子 and 窪田 宜夫 and 安藤 興一 and 岡安 隆一},
 issue = {3},
 journal = {Biochemical and Biophysical Research Communications},
 month = {Dec},
 note = {In order to investigate the mechanism of radio-sensitization by an Hsp90 inhibitor 17-Allylamino-17-demethoxygeldanamucin (17-AAG), we studied repair of DNA double strand breaks (DSBs) in irradiated human cells pre-treated with 17-AAG DSBs are thought to be the critical target for radiation-induced cell death. Two human tumor cell lines DU145 and SQ-5 which showed clear radio-sensitization by 17-AAG revealed a significant inhibition of DSB repair, while normal human cells which did not show radio-sensitization by the drug indicated no change in the DSB repair kinetics with 17AAG. We further demonstrated that BRCA2 was a novel client protein for Hsp90, and 17-AAG caused the degradation of BRCA2 and in turn altered the behavior of Rad51, a critical protein for homologous recombination (HR) pathway of DSB repair. Our data demonstrate for the first time that 17-AAG inhibits the HR repair process and could provide a new therapeutic strategy to selectively result in higher tumor cell killing.},
 pages = {658--663},
 title = {Inhibition of homologous recombination repair in irradiated tumor cells pretreated with Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin},
 volume = {351},
 year = {2006}
}