Double stranded breaks (DSBs), induced by ionizing radiation for example, is detected by a complex of sensor proteins including g-H2AX, 53BP1, MDC1, BRCA1, and the MRN complex (composed of MRE11, RAD50, and NBS1). Damage signals are then relayed to the central checkpoint mediator, ATM, which in turn activates Chk2 via phosphorylation and subsequent G₂ cell cycle arrest.

UV-induced DNA damage and replication stress is detected by an alternative set of sensor proteins including the 911 complex (composed of HUS1, RAD1, RAD9), RAD17 and RAD26, and subsequent signals are relayed to the central checkpoint mediator, ATR, which in turn activates Chk1 and either an inter S phase or G₂ cell cycle arrest. Cancer cells often adapt to DNA damaging chemotherapeutic agents as a means of escaping apoptosis. This adaptive mechanism may include cell cycle arrest and repair of damaged DNA. The checkpoint proteins are important in oncogenesis and, thus, a potential target for cancer therapy.

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