@article{oai:kanazawa-u.repo.nii.ac.jp:00027366,
 author = {小林, 昌彦 and 清水, 弘子 and 山本, 健一 and Kobayashi, Masahiko and Ono, Hirohito and Mihara, Keiko and Tauchi, Hiroshi and Komatsu, Kenshi and Shibata, Takashi and Shimizu, Hiroko and Uchida, Koji and Yamamoto, Ken-ichi},
 issue = {7},
 journal = {Genes to Cells},
 month = {Jul},
 note = {ATM (ataxia-telangiectasia mutated) is activated by a variety of noxious agent, including oxidative stress, and ATM deficiency results in an anomalous cellular response to oxidative stress. However, the mechanisms for ATM activation by oxidative stress remain to be established. Furthermore, it is not clear whether ATM responds to oxidative DNA damage or to a change in the intracellular redox state, independent of DNA damage. We found that ATM is activated by N-methyl-N′-nitro-nitrosoguanidine (MNNG) and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), in NBS1- or MSH6-deficient cells. We further found that ATM is activated by treating chromatin-free immunoprecipitated ATM with MNNG or 15d-PGJ2, which modifies free sulfhydryl (SH) groups, and that 15d-PGJ2 binds covalently to ATM. Interestingly, 15d-PGJ2-induced ATM activation leads to p53 activation and apoptosis, but not to Chk2 or H2AX phosphorylation. These results indicate that ATM is activated through the direct modification of its SH groups, independent of DNA damage, and this activation leads, downstream, to apoptosis. © 2006 The Authors Journal compilation © 2006 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd., がん研究所がん分子細胞制御},
 pages = {779--789},
 title = {ATM activation by a sulfhydryl-reactive inflammatory cyclopentenone prostaglandin},
 volume = {11},
 year = {2006}
}