Abstract
The ataxia telangiectasia mutated (ATM) protein kinase regulates the cellular response to deoxyribonucleic acid (DNA) double-strand breaks by phosphorylating numerous players in the extensive DNA damage response network. Two papers in this issue (Daniel et al. 2012. J. Cell Biol. http://dx.doi.org/10.1083/jcb201204035; Yamamoto et al. 2012. J. Cell Biol. http://dx.doi .org/10.1083/jcb201204098) strikingly show that, in mice, the presence of a catalytically inactive version of ATM is embryonically lethal. This is surprising because mice completely lacking ATM have a much more moderate phenotype. The findings impact on basic cancer research and cancer therapeutics. © 2012 Shiloh and Ziv.
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CITATION STYLE
Shiloh, Y., & Ziv, Y. (2012). The ATM protein: The importance of being active. Journal of Cell Biology, 198(3), 273–275. https://doi.org/10.1083/jcb.201207063
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