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Comment
. 2012 Aug 6;198(3):273-5.
doi: 10.1083/jcb.201207063.

The ATM protein: the importance of being active

Yosef Shiloh  1 , Yael Ziv
Affiliations
Comment

The ATM protein: the importance of being active

Yosef Shiloh et al. J Cell Biol. .

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.

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Figures

Figure 1.
Figure 1.
Phenotypic comparison of mouse Atm genotypes. Mice expressing an inactive protein as their sole source of Atm die in utero (Daniel et al., 2012; Yamamoto et al. 2012). Heterozygotes resemble wild-type (WT) animals, indicating lack of a dominant-negative effect. HRR, homologous recombination repair; kd, kinase dead.
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References

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