ATAXIA-TELANGIECTASIA MUTATED (ATM) is a serine/threonine protein
kinase that catalyzes the addition of a phosphate group to serine
or threonine residues and is activated upon perception of genotoxic
stresses (e.g. ionizing radiation). ATM primarily responds to
double stranded DNA breaks. The kinase phosphorylates histone
variant H2AX to form H2AXS139ph at double strand breaks. The
protein becomes activated in response to stress-induced damage in
somatic cells and DNA damage during meiosis. ATM has also been
implicated in cellular responses to telomere dysfunction. ATM works
synergistically with RUG3 during the DNA damage response.
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