Figure 2. The downstream effectors of the DDR. After activation by ATR, Chk1 phosphorylates the CDC25 family of phosphatases, thereby targeting them for ubiquityn-ation and subsequent degradation and preventing the activation of cyclin-dependent kinases. Chk2 is activated by ATM and phosphorylates p53, causing its stabilization and activation, while ATM also activates p53 directly. This in turn regulates the expression of the CDK inhibitor p21, leading to arrest of the cell cycle.