The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair

By C. Sørensen, L. Hansen, J. Dziegielewski, R. Syljuåsen, Cecilia Lundin, J. Bartek, Thomas Helleday. Nature Cell Biology, 2005

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Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair (2010, background): “In mammalian cells, the ATR- and Chk1-dependent checkpoint keeps replication foci active and prevents excessive DSB formation during replication blocks, suggesting that similar control mechanisms exist (Feijoo et al., 2001; Sorensen et al., 2005; Zachos et al., 2003).”
DNA damage sensing by the ATM and ATR kinases. (2013, background): “It was also suggested that when DSBs arise at stalled DNA replication forks, Chk1 phosphorylates the recombinase Rad51 and promotes repair of the break through HR (Sorensen et al. 2005).”
Regulation of homologous recombination in eukaryotes (2010, background): “DDR signaling is required for efficient DNA damage–induced HR (13, 108, 141).”
Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition. (2006, methodology): “2B) and used previously validated siRNA oligos to silence CHK1 protein expression (17).”