ArticleEMBO reports2010
A divalent FHA/BRCT-binding mechanism couples the MRE11-RAD50-NBS1 complex to damaged chromatin.
Article in EMBO reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Saccharomyces cerevisiae Xrs2 Binds DNA Through Its FHA Domain.Journal of molecular biology · 2025Article
- Identification of plants' functional counterpart of the metazoan mediator of DNA Damage checkpoint 1.EMBO reports · 2024Article
- The immediate-early protein 1 of human herpesvirus 6B interacts with NBS1 and inhibits ATM signaling.EMBO reports · 2024Article
- The molecular details of a novel phosphorylation-dependent interaction between MRN and the SOSS complex.Protein science : a publication of the Protein Society · 2023Article
- Species variations in XRCC1 recruitment strategies for FHA domain-containing proteins.DNA repair · 2022Article
- Phosphopeptide interactions of the Nbs1 N-terminal FHA-BRCT1/2 domains.Scientific reports · 2021Article
- Tumor Evolution and Therapeutic Choice Seen through a Prism of Circulating Tumor Cell Genomic Instability.Cells · 2021Review
- DNA folds threaten genetic stability and can be leveraged for chemotherapy.RSC chemical biology · 2021Review
- Mutation of Conserved Mre11 Residues Alter Protein Dynamics to Separate Nuclease Functions.Journal of molecular biology · 2020Article
- Treacle controls the nucleolar response to rDNA breaks via TOPBP1 recruitment and ATR activation.Nature communications · 2020Article
- MDC1 Interacts with TOPBP1 to Maintain Chromosomal Stability during Mitosis.Molecular cell · 2019Article
- NBS1 promotes the endonuclease activity of the MRE11-RAD50 complex by sensing CtIP phosphorylation.The EMBO journal · 2019Article
- Article
- A Novel Aspect of Tumorigenesis-BMI1 Functions in Regulating DNA Damage Response.Biomolecules · 2015Review
- Envisioning the dynamics and flexibility of Mre11-Rad50-Nbs1 complex to decipher its roles in DNA replication and repair.Progress in biophysics and molecular biology · 2015Review
- Structural studies of DNA end detection and resection in homologous recombination.Cold Spring Harbor perspectives in biology · 2014Review
- Functional deficiency of NBN, the Nijmegen breakage syndrome protein, in a p.R215W mutant breast cancer cell line.BMC cancer · 2014Article
- Article
- Structural mechanisms underlying signaling in the cellular response to DNA double strand breaks.Mutation research · 2013Review
- The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MRE11-RAD50-NBS1 (MRN) complex accumulates at sites of DNA double-strand breaks in large chromatin domains flanking the lesion site. The mechanism of MRN accumulation involves direct binding of the Nijmegen breakage syndrome 1 (NBS1) subunit to phosphorylated mediator of the DNA damage checkpoint 1 (MDC1), a large nuclear adaptor protein that interacts directly with phosphorylated H2AX. NBS1 contains an FHA domain and two BRCT domains at its amino terminus. Here, we show that both of these domains participate in the interaction with phosphorylated MDC1. Point mutations in key amino acid residues of either the FHA or the BRCT domains compromise the interaction with MDC1 and lead to defects in MRN accumulation at sites of DNA damage. Surprisingly, only mutation in the FHA domain, but not in the BRCT domains, yields a G2/M checkpoint defect, indicating that MDC1-dependent chromatin accumulation of the MRN complex at sites of DNA breaks is not required for G2/M checkpoint activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.