The DOI matches its Crossref record; 111 of the 112 references it cites were found in a registry or an index.
Assembly and function of DNA double-strand break repair foci in mammalian cells
Abstract
DNA double-strand breaks (DSBs) are among the most cytotoxic types of DNA damage, which if left unrepaired can lead to mutations or gross chromosomal aberrations, and promote the onset of diseases associated with genomic instability such as cancer. One of the most discernible hallmarks of the cellular response to DSBs is the accumulation and local concentration of a plethora of DNA damage signaling and repair proteins in the vicinity of the lesion, initiated by ATM-mediated phosphorylation of H2AX (γ-H2AX) and culminating in the generation of distinct nuclear compartments, so-called Ionizing Radiation-Induced Foci (IRIF). The assembly of proteins at the DSB-flanking chromatin occurs in a highly ordered and strictly hierarchical fashion. To a large extent, this is achieved by regulation of protein-protein interactions triggered by a variety of post-translational modifications including phosphorylation, ubiquitylation, SUMOylation, and acetylation. Over the last decade, insight into the identity of proteins residing in IRIF and the molecular underpinnings of their retention at these structures has been vastly expanded. Despite such advances, however, our understanding of the biological relevance of such DNA repair foci still remains limited. In this review, we focus on recent discoveries on the mechanisms that govern the formation of IRIF, and discuss the implications of such findings in light of our understanding of the physiological importance of these structures.
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“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 [9]
In the citing paper
“Full activation of ATM following DNA double-strand breaks requires Nbs1 of the MRN complex.9,11–13”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [9]
In the citing paper
“Phosphorylation of H2AX and S/T-Q sites, both of which are targets of ATM, occurs rapidly after DNA breaks.9,37,38”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [9]
Citations
Cites
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Jackson, S. P., & Bartek, J. (2009) · Nature · doi:10.1038/nature08467 · Cited by 6,092
DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139
Rogakou, E. P., Pilch, D. R., Orr, A. H., Ivanova, V. S., & Bonner, W. M. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.10.5858 · Cited by 5,438
Genome maintenance mechanisms for preventing cancer
Hoeijmakers, J. H. J. (2001) · Nature · doi:10.1038/35077232 · Cited by 3,939
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
Bakkenist, C. J., & Kastan, M. B. (2003) · Nature · doi:10.1038/nature01368 · Cited by 3,466
Megabase Chromatin Domains Involved in DNA Double-Strand Breaks in Vivo
Rogakou, E. P., Boon, C., Redon, C., & Bonner, W. M. (1999) · The Journal of Cell Biology · doi:10.1083/jcb.146.5.905 · Cited by 2,422
A genomic and functional inventory of deubiquitinating enzymes.
Nijman, S. M. B., Luna-Vargas, M. P. A., Velds, A., Brummelkamp, T. R., Dirac, A. M. G., Sixma, T. K., & Bernards, R. (2005) · Cell · doi:10.1016/j.cell.2005.11.007 · Cited by 1,854
Mechanism of Eukaryotic Homologous Recombination
Filippo, J. S., Sung, P., & Klein, H. L. (2008) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.77.061306.125255 · Cited by 1,766
The DNA Damage Response: Ten Years After
Harper, J. W., & Elledge, S. J. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.11.015 · Cited by 1,705
53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks
Bunting, S. F., Callén, E., Wong, N., Chen, H.-T., Polato, F., Gunn, A., Bothmer, A., Feldhahn, N., Fernandez-Capetillo, O., Cao, L., et al. (2010) · Cell · doi:10.1016/j.cell.2010.03.012 · Cited by 1,671
ATM Activation by DNA Double-Strand Breaks Through the Mre11-Rad50-Nbs1 Complex
Lee, J.-H., & Paull, T. T. (2005) · Science · doi:10.1126/science.1108297 · Cited by 1,424
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Douglas, P., Ye, R., Trinkle‐Mulcahy, L., Neal, J. A., Wever, V. D., MORRICE, N. A., Meek, K., & Lees‐Miller, S. P. (2014) · Bioscience Reports · doi:10.1042/bsr20140051 · Cited by 49
Carrillo, A. M., Hicks, M., Khabele, D., & Eischen, C. M. (2015) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-15-0089 · Cited by 31
Metadata
- Authors
- Bekker-Jensen, S., & Mailand, N.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Mailand, Niels
- ORCID
- Mailand, Niels
- Venue
- DNA Repair
- Publisher
- Elsevier BV
- Published
- 2010-12
- Volume
- 9
- Issue
- 12
- Pages
- 1219-1228
- ISSN
- 1568-7856 (ISSN-L)
- 1568-7864
- OpenAlex
- W1999541392
- Cited by
- 338
- References
- 112
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 6 · 2023: 8 · 2022: 11 · 2021: 17 · 2020: 16 · 2019: 14 · 2018: 16 · 2017: 24 · 2016: 21 · 2015: 33 · 2014: 45 · 2013: 36 · 2012: 45
- FWCI
- 3.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- DNA repair (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Lundbeckfonden
- Novo Nordisk Fonden
- Kræftens Bekæmpelse
- Sundhed og Sygdom, Det Frie Forskningsråd
- 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 › Genomics and Chromatin Dynamics
- Keywords
- DNA double-strand break repair, ionizing radiation-induced foci, DNA damage signaling, γH2AX, protein-protein interaction, post-translational modification, ubiquitination, SUMOylation, acetylation, chromatin assembly, genomic instability, mammalian cells
- MeSH terms
- Tumor Suppressor p53-Binding Protein 1, Animals, Cell Nucleus, Chromatin, DNA Repair, DNA-Binding Proteins, Histones, Humans, Nuclear Proteins, Phosphorylation, Protein Processing, Post-Translational, Trans-Activators, Cell Cycle Proteins, BRCA1 Protein, Guanine Nucleotide Exchange Factors, Genomic Instability, Ubiquitin-Protein Ligases, Multiprotein Complexes, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, DNA Breaks, Double-Stranded, Ubiquitination
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