Mammalian G1- and S-phase checkpoints in response to DNA damage.

By J. Bartek, J. Lukas. Current Opinion in Cell Biology, 2001

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From polyploidy to aneuploidy, genome instability and cancer (2004, background): “pl?P04637">p53 (a tumour suppressor protein with a well-characterized role in DNA-damage checkpoint”
ATM Activation by Oxidative Stress (2010, background): “Activation of cell cycle checkpoints is another hallmark of DDR [28, 29].”
ATM and related protein kinases: safeguarding genome integrity (2003, background): “A hallmark of this response is the activation of CELL-CYCLE CHECKPOINTS”
The impact of a negligent G2/M checkpoint on genomic instability and cancer induction (2007, background): “Interestingly, the p53-dependent G1 checkpoint does not require activation of the CDC25 phosphatases by the CHK1/2 kinases, raising the possibility that this may represent the insensitive step of checkpoint signallin”
The cell cycle and seed germination (2003, background): “In yeast and mammalian cells, it has been established clearly that DNA damage blocks the establishment or progression of the S phase until damaged DNA has been repaired (Rhind and Russell, 2000; Bartek and Lukas, 2001).”
Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “Also undetermined is whether these two checkpoint cascades can occur independently; that is, can limited damage that requires little time for repair induce only the posttranslational cascade for a brief delay, or are both cascades always activated together, regardless of the extent of damage (12)? W”