Cell Cycle / Checkpoint Control

The Nijmegen breakage syndrome (NBS) is characterized by defects in cell cycle checkpoints, growth retardation, an increased propensity for cancer and sensitivity to ionizing radiation (1). Repair of DNA double-strand breaks by radiation is dependent on a multifunctional complex containing Rad50, Mre11 and the NBS1 gene product p95/NBS1 (also called p95 or nibrin) (2). p95/NBS1 is a protein with a forkhead-associated domain and a carboxy-terminal repeat frequently found in cell cycle regulatory and DNA repair proteins (1,3). The overlap between clinical and cellular phenotypes in ataxia telangiectasia (AT) and NBS suggests that AT-mutated (ATM) and p95/NBS1 function in the same biochemical pathway. ATM interacts with and phosphorylates p95/NBS1 at Ser343 after exposure to ionizing radiation (4-7).

1. Varon, R. et al. (1998) Cell 93, 467-476.
2. Carney, J. P. et al. (1998) Cell 93, 477-486.
3. Durocher, D. et al. (1999) Mol. Cell 4, 387-394.
4. Gatei, M. et al. (2000) Nat. Genet. 25, 115-119.
5. Lim, D. S. et al. (2000) Nature 404, 613-617.
6. Wu, X. et al. (2000) Nature 405, 477-482.
7. Zhao, S. et al. (2000) Nature 405, 473-477.

• Lukas, C. et al. (2003) Distinct spatiotemporal dynamics of mammalian checkpoint regulators induced by DNA damage. Nat. Cell Biol. 5, 255-260. Applications: IC-IF Western Blotting

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Phospho-p95/NBS1 (Ser343) Antibody

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