Checkpoint Rad proteins function early in the DNA damage signaling cascade to arrest cell cycle progression in response to DNA damage (1). There is a direct regulatory linkage between the Rad17 homologue and the checkpoint kinases, ATM and ATR (2). ATR but not ATM phosphorylates the Rad17 checkpoint protein on Ser635 and Ser645 in vitro. In undamaged synchronized human cells, these two sites were phosphorylated in late G(1), S, and G(2)/M, but not in early-mid G(1). Treatment of cells with genotoxic stress induced phosphorylation of Rad17 in cells in early-mid G(1). This suggests that ATR and Rad17 are essential components of a DNA damage response pathway in mammalian cells (3).
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