Ataxia telangiectasia mutated (ATM) is a serine/threonine protein kinase that is recruited and activated by DNA double-strand breaks. It phosphorylates several key proteins that initiate activation of the DNA damage checkpoint, leading to cell cycle arrest, DNA repair or apoptosis. Several of these targets, including p53, CHK2 and H2AX are tumor suppressors. The protein is named for the disorder Ataxia telangiectasia caused by mutations of ATM.
Pathway
ATM mediated phosphorylation of repair proteins; ATM mediated response to DNA double-strand break; Apoptosis; Autodegradation of the E3 ubiquitin ligase COP1; BARD1 signaling events; BRCA1-associated genome surveillance complex (BASC); Canonical NF-kappaB
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