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. 2017 Dec 14;46(2):730–747. doi: 10.1093/nar/gkx1240

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© The Author(s) 2017. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — PABPN1 is a novel ATM substrate in the DSB response. ATM dependence of PABPN1 phosphorylation following NCS treatment. U2-OS cells were treated with 20 ng/ml of NCS, with or without 30 min pretreatment with 10 μM of the chemical ATM inhibitor, KU-55933. Cellular extracts were subjected to western blotting analysis with the indicated antibodies. Phosphorylated KAP-1 (57) served as control for DNA damage induction and response. PAPBN1 phosphorylation following NCS treatment is independent of ATR or DNA-PK. U2-OS cells were treated with 20 ng/ml of NCS, with or without pretreatment with the chemical inhibitors NU7441 (DNA-PK inhibitor-10 μM) or AZ20 (ATR inhibitor-0.5 μM). Cellular extracts were subjected to immunoblotting analysis with the indicated antibodies. Phosphorylated KAP-1 served as control for DNA damage induction and response.