Signal transduction, such as the transmission of a signal through protein modifications, is essential for the cell to cope with stress. A good example of stress signaling is the DNA damage response (DDR). Cells have adapted the DDR as a way for the normal functions, such as those involved in cell cycle progression, to temporarily shut down while stress-induced damage is repaired. Depending on the cell cycle phase of the cell at the time of damage, the cell can halt cell cycle progression by eliciting checkpoints (1, 2). However, if the damage is not repairable, then the cell may trigger apoptosis. Apoptosis and cell cycle arrest are crucial, since cells that have dysfunctional checkpoint and apoptotic responses are able to replicate despite persistent damage, potentially leading to mutations and tumor formation. Therefore, the existence of signaling proteins responsible for the initiation of cell cycle arrest during damage repair or apoptosis if the damage cannot be repaired implies the existence of mechanisms for suppressing these pathways upon the completion of repair to allow the resumption of normal cell cycle progression. The
