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Nature 431, 997-1002 (21 October 2004) | doi:10.1038/nature02989;
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Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells
The |[lsquo]|ataxia telangiectasia mutated|[rsquo]| (Atm) gene maintains genomic stability by activating a key cell-cycle checkpoint in response to DNA damage, telomeric instability or oxidative stress. Mutational inactivation of the gene causes an autosomal recessive disorder, ataxia–telangiectasia, characterized by immunodeficiency, progressive cerebellar ataxia, oculocutaneous telangiectasia, defective spermatogenesis, premature ageing and a high incidence of lymphoma.
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Abstract
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