ArticleMolecular and cellular biology2001
Distinct functional domains of nibrin mediate Mre11 binding, focus formation, and nuclear localization.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 192 citations in OpenAlex.
- Biochemical Mechanisms of Genetic Recombination and DNA Repair.Annual review of biochemistry · 2025Review
- MRE11 is essential for the long-term viability of undifferentiated spermatogonia.Cell proliferation · 2024Article
- Cancer and Radiosensitivity Syndromes: Is Impaired Nuclear ATM Kinase Activity the Primum Movens?Cancers · 2022Review
- NBS1 is required for SPO11-linked DNA double-strand break repair in male meiosis.Cell death and differentiation · 2020Article
- Functional and structural insights into the MRX/MRN complex, a key player in recognition and repair of DNA double-strand breaks.Computational and structural biotechnology journal · 2020Review
- NBS1 promotes the endonuclease activity of the MRE11-RAD50 complex by sensing CtIP phosphorylation.The EMBO journal · 2019Article
- Repair of protein-linked DNA double strand breaks: Using the adenovirus genome as a model substrate in cell-based assays.DNA repair · 2019Article
- Processing of DNA Double-Strand Breaks by the MRX Complex in a Chromatin Context.Frontiers in molecular biosciences · 2019Review
- Purification and Biophysical Characterization of the Mre11-Rad50-Nbs1 Complex.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Assembling the Human Resectosome on DNA Curtains.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Review
- Xrs2 and Tel1 Independently Contribute to MR-Mediated DNA Tethering and Replisome Stability.Cell reports · 2018Article
- Identification of variants in pleiotropic genes causing "isolated" premature ovarian insufficiency: implications for medical practice.European journal of human genetics : EJHG · 2018Article
- Nm23-H1 is involved in the repair of ionizing radiation-induced DNA double-strand breaks in the A549 lung cancer cell line.BMC cancer · 2018Article
- Mre11-Rad50-dependent activity of ATM/Tel1 at DNA breaks and telomeres in the absence of Nbs1.Molecular biology of the cell · 2018Article
- Article
- Eukaryotic resectosomes: A single-molecule perspective.Progress in biophysics and molecular biology · 2017Review
- The Mre11-Nbs1 Interface Is Essential for Viability and Tumor Suppression.Cell reports · 2017Article
- An Intrinsically Disordered Region of the DNA Repair Protein Nbs1 Is a Species-Specific Barrier to Herpes Simplex Virus 1 in Primates.Cell host & microbe · 2016Article
- Structural mechanism of ATP-dependent DNA binding and DNA end bridging by eukaryotic Rad50.The EMBO journal · 2016Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The inherited chromosomal instability disorder Nijmegen breakage syndrome (NBS) results from truncating mutations in the NBS1 gene, which encodes the protein nibrin. Nibrin is part of a nuclear multiprotein complex that also contains the DNA repair proteins Mre11 and Rad50. Upon irradiation, this complex redistributes within the nucleus, forming distinct foci that have been implicated as sites of DNA repair. In NBS cells, nibrin is absent and Mre11 and Rad50 are cytoplasmic. In this study, the interacting domains on nibrin and Mre11 were mapped using the yeast two-hybrid system and expression of epitope-tagged constructs in NBS fibroblasts. Deletion of the carboxy-terminal 101 amino acids of nibrin eliminated its ability to interact with Mre11 and to complement the radiation sensitivity of NBS cells. However, this truncated form of nibrin could localize to the nucleus and form radiation-inducible foci. Expression of a carboxy-terminal 354-amino-acid fragment of nibrin was sufficient to direct the nuclear localization of nibrin, as well as that of Mre11 and Rad50. Despite providing some partial complementation of the radiation-sensitive phenotype, the nibrin-Mre11-Rad50 complexes in these cells were unable to form foci. These results indicate that nibrin directs not only the nuclear localization of the nibrin-Mre11-Rad50 complexes but also radiation-induced focus formation. However, direct interaction between nibrin and Mre11 is required for normal cellular survival postirradiation. Distinct domains of nibrin are required for each of these functions, focus formation, nuclear localization, and Mre11 interaction.
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