Accumulation of DNA damage has been associated with the onset of senescence and the predisposition to cancer. The gene responsible for ataxia telangiectasia (A-T) is ATM (Ataxia-telangiectasia mutant), a master controller of cellular pathways and networks, orchestrating the response to a specific type of DNA damage, i.e., the double strand break. It has now been demonstrated that mutations in ATM lead to defective telomere maintenance in mammalian cells. This review will focus on its roles in telomere metabolism and how ATM and telomeres serve as controllers of cellular responses to DNA damage.
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