ATR-Mediated Checkpoint Pathways Regulate Phosphorylation and Activation of Human Chk1

By Hui Zhao, H. Piwnica-Worms. Molecular and Cellular Biology, 2001

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Molecular mechanisms of cisplatin resistance (2012, background): “…checkpoint kinase 1 (CHEK1, the most prominent substrate and downstream effector of ATR), which in turn phosphorylates the tumor suppression protein TP53 on serine 20, allowing for its stabilization (Shieh et al., 2000; Appella and Anderson, 2001; Damia et al., 2001; Zhao and Piwnica-Worms, 2001).”
The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair (2005, background): “It is phosphorylated and activated by the kinase AT”
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis (2005, background): “4c ); of which Ser 345 is regarded as a preferential target for phosphorylation by AT”
ATM and related protein kinases: safeguarding genome integrity (2003, background): “For example, whereas CHK2 is a preferred ATM substrate in the cell-cycle-checkpoint pathways, CHK1 is a preferred ATR target in the G2–M checkpoint pathwa”
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, result): “Activation of MK2 by cisplatin, camptothecin, and doxorubicin is strikingly similar to the activation profile reported for Chk1 (Agner et al., 2005; Ho et al., 2005; Mailand et al., 2000; Zhao and Piwnica-Worms, 2001).”