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ATM function and telomere stability

Abstract

Accumulation of DNA damage has been associated with the onset of senescence and 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 responses to a specific type of DNA damage: the double strand break. Based on the homology of the human ATM gene to the TEL1, MEC1 and rad3 genes of yeast, it has now been demonstrated that mutations in ATM lead to defective telomere maintenance in mammalian cells. While ATM has both nuclear and cytoplasmic functions, 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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Acknowledgements

I am grateful to the members of my laboratory for the comments on this manuscript. I regret being unable to cite many papers due to limited space. This work was supported by grants from the National Institute of Health (NS34746) and A-T Children's Project.

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Correspondence to Tej K Pandita.

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Pandita, T. ATM function and telomere stability. Oncogene 21, 611–618 (2002). https://doi.org/10.1038/sj.onc.1205060

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