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. 2017 Jun 30;38(2):693–702. doi: 10.3892/or.2017.5773

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Copyright: © Nakajima et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Limited responsiveness of MICA/B expression is observed in insensitive cell lines independent of the type of DNA damage. (A) Carbon IR, which produces complex DNA damage, induced MICA/B expression in U2OS (sensitive), but not in T98G and A549 (insensitive) cells. MICA/B expression was analyzed by FACS 24 h after 10 Gy carbon IR. (B) Carbon IR effectively induces DNA damage signaling. Phosphorylation of Chk1 S345 in A549 cells was examined by immunoblotting. (C) Phosphorylation of Chk1 S345 in A549 cells is ATM/ATR-dependent after both X-rays and carbon IR. (D) A similar response to MICA/B expression in T98G (insensitive) and SaOS2 (sensitive) cells was observed after treatment with aphidicolin, a DNA polymerase inhibitor, which induces DNA replication damage in the S phase. (E) Fold increase in aphidicolin-induced MFI from the experiment described in D. Similar results were obtained in >2 independent experiments in all panels.