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. 2022 Oct 6;10:1020643. doi: 10.3389/fcell.2022.1020643

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Copyright © 2022 Yam, Lim and Surana.

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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Activation of DNA damage checkpoint and cell cycle arrest in mammalian cells. The DSBs in mammalian cells are recognized by MRN complex and processed with the help of CtIP, EXO1, BLM, and DNA2 proteins to generate 3′ ssDNA extension. This results in the recruitment and activation of ATM/ATR kinase and subsequently, the activation of CHK/CHK2 kinases. The activated kinases then inhibit the effectors required for the onset of mitosis, thus causing cells to arrest in G2. In addition, ATR/ATM/CHK1/CHK2 kinases stabilize p53 which help in the imposition of G2 arrest. P53 also activates apoptotic pathway in certain cellular contexts. As in yeast, the activation of checkpoint effectors in mammalian cells also trigger the DNA repair pathways.