ATM
Ataxia telangiectasia mutated (ATM; EC 2.7.11.1) kinase recognizes and signals to double-strand breaks (DSB), which are among the most critical lesions in chromosomal DNA[1],[2]. ATM is present in the nucleus as an inactive dimer or oligomer, and is activated in response to DSBs in a process that involves autophosphorylation. This causes a dissociation of the dimer to form active monomeric forms, which are able to initiate the phosphorylation of many intermediates, such as p53 and the checkpoint kinase CHK2, which are involved in DNA repair and cell-cycle control[3].
Ataxia telangiectasia kinase subclasses: ATM, ATR
[1] DNA-PK, theDNA-activated protein kinase, is differentially expressed in normal and malignant human tissues. U Moll, RLau,MA Sypes, MM Gupta,CW Anderson. Oncogene 1999, 18, 3114-3126.
[2] ATM and theDNA damage response. Workshop on ataxia-telangiectasia and related syndromes. Lavin MF, Delia D, Chessa L.EMBO Rep. 2006, 7, 154–160.
[3] DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation. Bakkenist CJ,KastanMB. Nature. 2003, 421, 499-506.