Abstract
The ATM gene and its protein product have recently become a focus of interest for clinicians, biologists and cancer epidemiologists. The ATM protein is involved in a complex junction of signal transduction pathways linking cellular stress responses, cell cycle control and specific developmental processes (1). The ATM gene was identified by virtue of its responsibility for a human genetic disorder, ataxia- telangiectasia (A-T). A-T is an autosomal recessive disease characterized by cerebellar degeneration, immunodeficiency, premature aging, cancer predisposition and radiation sensitivity. A-T cells exhibit chromosomal instability, extreme sensitivity to ionizing radiation and radiomimetic chemicals, defective cell cycle checkpoints, and defects in several signal transduction pathways that respond to mitogenic stimuli and genotoxic stress (see refs. 1, 2 for recent reviews).
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Shiloh, Y., Bar-Shira, A., Galanty, Y., Ziv, Y. (1998). Cloning and Expression of Large Mammalian cDNAs: Lessons from ATM. In: Setlow, J.K. (eds) Genetic Engineering. Genetic Engineering, vol 20. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1739-3_12
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