The MRE11 complex: starting from the ends
Open accessAbstract
The maintenance of genome stability depends on the DNA damage response (DDR), which is a functional network comprising signal transduction, cell cycle regulation and DNA repair. The metabolism of DNA double-strand breaks governed by the DDR is important for preventing genomic alterations and sporadic cancers, and hereditary defects in this response cause debilitating human pathologies, including developmental defects and cancer. The MRE11 complex, composed of the meiotic recombination 11 (MRE11), RAD50 and Nijmegen breakage syndrome 1 (NBS1; also known as nibrin) proteins is central to the DDR, and recent insights into its structure and function have been gained from in vitro structural analysis and studies of animal models in which the DDR response is deficient.
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The MRN complex senses and processes double-strand DNA breaks and activates downstream DNA damage response proteins such as ATM.
“The MRN complex is important in sensing and processing double-strand DNA breaks, as well as activating downstream DNA damage response proteins that mediate or signal for DNA repair, such as the DNA damage-induced kinase ATM.9–13”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [10]
Patients with congenital mutations in DNA repair proteins such as NBS1 and ATM have increased chromosomal fragility and increased incidence of tumor formation.
“This is evident in patients with congenital mutations in DNA repair proteins, such as NBS1 and ATM. Cells from these patients have increased chromosomal fragility, and the patients themselves have an increased incidence of tumor formation.10,16,17”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [10]
Altered DNA repair is a significant contributing factor to genomic instability.
“altered DNA repair has been implicated as a significant contributing factor.10”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [10]
Genome instability can precede tumor formation, characterizes malignant cells, and is associated with defective DNA damage responses.
“Genome instability can be a precursor to tumor formation, is a hallmark of malignant cells, and is connected with impairments in the DNA damage response.10,15”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [10]
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Mechanisms of DNA damage, repair, and mutagenesis
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Hirsch, M. L. (2015) · Gene Therapy · doi:10.1038/gt.2014.109 · Cited by 32 · see citing works
A nervous predisposition to unrepaired DNA double strand breaks
Reynolds, J. J., & Stewart, G. S. (2013) · DNA Repair · doi:10.1016/j.dnarep.2013.04.011 · Cited by 26 · see citing works
Protecting the genome from mdm2 and mdmx
Melo, A. N., & Eischen, C. M. (2012) · Genes & Cancer · doi:10.1177/1947601912454139 · Cited by 20 · see citing works
- Authors
- Stracker, T. H., & Petrini, J. H. J.
- Affiliations
- Institute for Research in Biomedicine (ES)
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Stracker, Travis H.
- Petrini, John H. J.
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2011-01-21
- Volume
- 12
- Issue
- 2
- Pages
- 90-103
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- PMC
- PMC3905242
- OpenAlex
- W1971419576
- Cited by
- 734
- References
- 173
- Citations by year
- 2026: 26 · 2025: 32 · 2024: 27 · 2023: 32 · 2022: 42 · 2021: 33 · 2020: 52 · 2019: 51 · 2018: 49 · 2017: 39 · 2016: 58 · 2015: 67 · 2014: 76 · 2013: 83 · 2012: 41
- FWCI
- 6.53
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Geoffrey Beene Foundation
- National Institutes of Health
- National Cancer Institute (R13CA162528, P30CA008748)
- National Institute of General Medical Sciences (R37GM059413, R01GM059413, R01GM056888)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- Mre11 complex, DNA double-strand break repair, DNA damage response, genome stability, MRE11, RAD50, NBS1, meiotic recombination, protein complex structure, DNA repair, cancer susceptibility
- MeSH terms
- Animals, DNA Repair, DNA-Binding Proteins, Humans, Pyrococcus furiosus, DNA Repair Enzymes, DNA Breaks, Double-Stranded
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