The essential kinase ATR: ensuring faithful duplication of a challenging genome
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Molecular Biology
Link
http://www.nature.com/articles/nrm.2017.67.pdf
Reference168 articles.
1. Zeman, M. K. & Cimprich, K. A. Causes and consequences of replication stress. Nat. Cell Biol. 16, 2–9 (2014).
2. Brown, E. J. & Baltimore, D. ATR disruption leads to chromosomal fragmentation and early embryonic lethality. Genes Dev. 14, 397–402 (2000).
3. de Klein, A. et al. Targeted disruption of the cell-cycle checkpoint gene ATR leads to early embryonic lethality in mice. Curr. Biol. 10, 479–482 (2000). References 2 and 3 demonstrate that ATR is essential for viability in vivo.
4. O'Driscoll, M., Ruiz-Perez, V. L., Woods, C. G., Jeggo, P. A. & Goodship, J. A. A splicing mutation affecting expression of ataxia-telangiectasia and Rad3-related protein (ATR) results in Seckel syndrome. Nat. Genet. 33, 497–501 (2003).
5. Cimprich, K. A., Shin, T. B., Keith, C. T. & Schreiber, S. L. cDNA cloning and gene mapping of a candidate human cell cycle checkpoint protein. Proc. Natl Acad. Sci. USA 93, 2850–2855 (1996).
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