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. 2020 Sep 8;8:539485. doi: 10.3389/fcell.2020.539485

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Copyright © 2020 He, Li, Xu, Ru, Huang, Lin and Peng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic representation of the AMPK-mediated G2 arrest regulation and DNA damage in mouse zygotes under mild oxidative stress. Oxidative stress activated AMPK first in the cytoplasm, which is subsequently translocated in the nucleus. AMPK activation contributes to oxidative stress-induced G2 arrest, by inhibiting CDK1 activity via the upregulation protein level of p53 and p21. The G2 arrest facilitates DNA damage repair and the development and survival of oxidative stress-damaged embryos.