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. Activity of ATM protein is under tight control, and mutation of ATM can cause disease such as Ataxia telangiectasia (AT) and cancers.
Pathway
ATM mediated phosphorylation of repair proteins; Apoptosis; Autodegradation of the E3 ubiquitin ligase COP1; BRCA1-associated genome surveillance complex (BASC)
Citations
Publication ()
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