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. 2018 Jun 25;46(15):7662–7674. doi: 10.1093/nar/gky536

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© The Author(s) 2018. 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. — Induction of EVI1 double phosphorylation by DNA damage. (A) Immunoprecipitated EVI1 from SB1690CB cells probed with anti-pS860-EVI1 (upper panel), and anti-pS858/pS860-EVI1 antibody, untreated (lane 1), and after 1 and 2 h (lane 2 and 3) post radiation. (B) Western blot (WB) of EVI1-immunoprecipitates from untreated (lanes 1 and 2) and irradiated (lanes 3 and 4) SB1690CB cells pre-treated (1 h) with 10 μM ATM-kinase inhibitor KU55933 (lanes 2 and 4), and not pre-treated (lanes 1 and 3). Membranes were probed for doubly phosphorylated EVI1 with anti-pS858/pS860-EVI1 antibody. Middle panel: membrane as upper panel re-probed with pan-EVI1 antibody. Lower panel: WB of p-p53 (Ser15) carried out on input samples as positive control for ATM-activity and ATM-inhibition.