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Article

A divalent FHA/BRCT-binding mechanism couples the MRE11-RAD50-NBS1 complex to damaged chromatin.

EMBO reports - 1 May 2010

Hari Flurina J, Spycher Christoph, Jungmichel Stephanie, Pavic Lucijana, Stucki Manuel

Abstract excerpt

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...

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Share to Acid Anhydride Hydrolases
Share to Adaptor Proteins, Signal Transducing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromatin

Share to DNA Breaks, Double-Stranded

Share to DNA Repair Enzymes

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Share to MRE11 Homologue Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 20224574
DOI: 10.1038/embor.2010.30
PMCID: PMC2868538

Genes

MDC1
MRE11
RAD50

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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A divalent FHA/BRCT-binding mechanism couples the MRE11-RAD50-NBS1 complex to damaged chromatin.PMID 20224574Read ↗

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Mre11–Rad50–Nbs1 is a keystone complex connecting DNA repair machinery, double-strand break signaling, and the chromatin templateThis paper is one of a selection of papers published in this Special Issue, entitled 28th International West Coast Chromatin and Chromosome Conference, and has undergone the Journal's usual peer review process.Semantic proximity Read ↗

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