Anti-Human ATM

DNA double strand breaks represent a major threat to an organism’s genome. Eukaryotic cells have developed mechanisms that sense the presence this damage and initiate suitable responses that can include DNA repair, cell cycle delay, and programmed cell death (1). The ATM (mutated in Ataxia-Telangiectasia) protein kinase is activated following th e formation of DNA double strand breaks, phosphorylating p53 and another kinase CHK2 (2). This initiates a signaling cascade leading to the phosphorylation and inhibition of Cdc25, ultimately preventing cell cycle progression. In some cell types, such as the hemapoietic system, this leads to apoptosis instead of cell cycle arrest. Multiple isoforms of ATM are known to exist.