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. 2019 Nov 6;46(4):375–390. doi: 10.1111/nan.12584

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© 2019 The Authors. Neuropathology and Applied Neurobiology published by John Wiley & Sons Ltd on behalf of British Neuropathological Society

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Suppression of apurinic/apyrimidinic endonuclease 1 (APE1) activity or knockdown of APE1 reduces phosphorylated p53‐binding protein 1 (53BP1) foci in the nuclei of rat cortical neurons subjected to oxidative stress. (A) Phosphorylated 53BP1 foci (green) were dramatically repressed when APE1 activity was inhibited following menadione treatment. APE1 (red) accumulation appeared immediately and persisted in the nuclei (blue) for at least 24 h (scale bar: 50 nm). (B) Quantitation of the data in (A). (C) Immunoblotting images showed that the levels of phosphorylated 53BP1 foci (green) significantly decreased in APE1‐knockdown neurons (scale bar: 10 nm). (D) Quantitation of the data in (C). Data are shown as means ± SE (n = 3).