@article{oai:repo.qst.go.jp:00046214,
 author = {Lee, Kyung-Jong and Yajima, Hirohiko and et.al and 矢島 浩彦},
 issue = {14},
 journal = {The Journal of Biological Chemistry},
 month = {Apr},
 note = {The catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) plays an important role in DNA double-strand break (DSB) repair as the underlying mechanism of the non- homologous end joining pathway. When DSBs occur, DNA- PKcs is rapidly phosphorylated at both the Thr-2609 and Ser- 2056 residues, and such phosphorylations are critical for DSB repair. In this study we report that, in addition to responding to DSBs, DNA-PKcs is activated and phosphorylated in normal cell cycle progression through mitosis. Mitotic induction of DNA- PKcs phosphorylation is closely associated with the spindle apparatus at centrosomes and kinetochores. Furthermore, depletion of DNA-PKcs protein levels or inhibition of DNA- PKcs kinase activity results in the delay of mitotic transition because of chromosome misalignment. These results demon- strate for the first time that DNA-PKcs, in addition to its role in DSB repair, is a critical regulator of mitosis and could modulate microtubule dynamics in chromosome segregation.},
 pages = {12796--12802},
 title = {Involvement of DNA-dependent protein kinase in normal cell cycle progression through mitosis},
 volume = {286},
 year = {2011}
}