Extensive studies have revealed its dual role in locally promoting detection and repair of DSBs as well as in activating global DNA damage checkpoints.
DNA damage checkpoints occur at the G1/S and G2/M boundaries.
In contrast to Drosophila cleavage cycles, Xenopus cleavage cycles are found to lack DNA damage checkpoints.
The replication checkpoint and S-phase DNA damage checkpoints are mechanistically closely related.
Thus, DNA damage checkpoints are not fully functional during mitosis, even if they exist [13], [14].
DNA damage checkpoints insure that the integrity of genomic DNA is faithfully maintained throughout the eukaryotic cell cycle.
G2-phase functions for Plk1, including recovery from DNA damage checkpoints, are supported by several studies [18] [21].
Induction of senescence by oncogenic RAS involves activation of DNA damage checkpoints and is mediated by p53 [25], [25].
Cells were treated with phleomycin to activate G1/S and G2/M DNA damage checkpoints.
These data revealed specific differences in the signalling pathways of the decatenation and DNA damage checkpoints.
We next examined a network of proteins responsible for DNA damage checkpoints following exposure to pemetrexed.
