ATM (Ataxia telangiectasia mutated) is a serine/threonine protein kinase which is recruited and activated by DNA double strand breaks. ATM phosphorylation of several key proteins causes the initial activation of the DNA damage checkpoint directing the cell to cell cycle arrest, DNA repair or programmed cell death. Several of these targets (p53, CHK2 and H2AX) are tumour suppressors. Cambridge Bioscience offers a range of tools including antibodies and peptides to study ATM and inter-related pathways.
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