Abstract
The ataxia-telangiectasia-mutated (ATM) and ataxia-telangiectasia-mutated and Rad3-related (ATR) DNA damage repair pathways serve as the surveillance system which keeps a check on different types of DNA damages and lesions, which includes DNA single-strand breaks, DNA double-strand breaks and other aberrant structures such as arrested replication forks during replication. The ATM and ATR kinases belong to PIKK class of kinases which activate a large number of downstream mediator and effector molecules. The main classes of effector kinases activated by ATM and ATR are checkpoint kinase 2 and checkpoint kinase 1, respectively. ATR works primarily with the RAD9-RAD1-HUS1 (9-1-1) complex, whereas ATM works with the MRE11– RAD50–NBS1 complex. Together ATM and ATR kinase protects the cells' genomic integrity and prevents random mutations to be carried into their progeny.
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