@article{oai:nagasaki-u.repo.nii.ac.jp:00014590,
 author = {Ariyoshi, Kentaro and Suzuki, Keiji and Goto, Makoto and Oshimura, Mitsuo and Ishizaki, Kanji and Watanabe, Masami and Kodama, Seiji},
 issue = {3},
 journal = {Journal of Radiation Research},
 month = {May},
 note = {Werner syndrome (WS) is an autosomal recessive disease characterized by premature aging and caused by mutations of the WRN gene mapped at 8p12. To examine functional complementation of WS phenotypes, we introduced a normal human chromosome 8 into a strain of WS fibroblasts (WS3RGB) immortalized by expressing a human telomerase reverse transcriptase subunit (hTERT) gene. Here, we demonstrate that the abnormal WS phenotypes including cellular sensitivities to 4-nitroquinoline-1-oxide (4NQO) and hydroxy urea (HU), and chromosomal radiosensitivity at G2 phase are corrected by expression of the WRN gene mediated by introducing a chromosome 8. This indicates that those multiple abnormal WS phenotypes are derived from a primary, but not secondary, defect in the WRN gene., Journal of radiation research, 50(3), pp.253-259; 2009},
 pages = {253--259},
 title = {Introduction of a Normal Human Chromosome 8 Corrects Abnormal Phenotypes of Werner Syndrome Cells Immortalized by Expressing an hTERT Gene},
 volume = {50},
 year = {2009}
}