To function properly, cell-cycle checkpoints require sensors of DNA damage, signal transducers, and effector molecules. The sensors and transducers of DNA damage appear to be similar for the G1/S and G2/M checkpoints.
They include, as sensors, proteins of the RAD family and ataxia telangiectasia mutated (ATM) and as transducers, the CHK kinase families. The checkpoint effector molecules differ, depending on the cell-cycle stage at which they act.
In the G1/S checkpoint, cell-cycle arrest is mostly mediated through p53, which induces the cell-cycle inhibitor p21. Arrest of the cell cycle by the G2/M checkpoint involves both p53-dependent and independent mechanisms.
Defect in cell-cycle checkpoint components is a major cause of genetic instability in cancer cells.
References
Zou, L.; Elledge, S. J. : Sensing DNA damage through ATRIP recognition of RPA-ssDNA complexes. Science 300: 1542-1548, 2003. PubMed ID : 12791985