Nibrin (Nijmegen breakage syndrome protein 1, NBS1) contains 2 modules found in cell cycle check point; a forkhead-associated domain and a BRCA1 C-teminal repeat (1). In mammalian cells, Nibrin forms a complex with Mre11 and Rad50 (MRN). Nuclear localization of the MRN complex is relevant for chromosomal stability, meiotic recombination, DNA repair and telomere maintenance in eukaryotic cells. Mutation in Nibrin and Mre11 causes respectively two related disorders, Nijmegen breakage syndrome (NBS) and Ataxia-Telangiectasia- like disorder (ATLD) (2-4). Nibrin is phosphorylated at Serine 343 by ATM. The in vivo modification of these residues is essential for the cellular response to DNA damage, including an S-phase checkpoint activation, formation of the NBS1/Mrel1/Rad50 nuclear foci and rescue of hypersensitivity to ionizing radiation (5).
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