The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Activation of the Cellular DNA Damage Response in the Absence of DNA Lesions
Open accessAbstract
The cellular DNA damage response (DDR) is initiated by the rapid recruitment of repair factors to the site of DNA damage to form a multiprotein repair complex. How the repair complex senses damaged DNA and then activates the DDR is not well understood. We show that prolonged binding of DNA repair factors to chromatin can elicit the DDR in an ATM (ataxia telangiectasia mutated)– and DNAPK (DNA-dependent protein kinase)–dependent manner in the absence of DNA damage. Targeting of single repair factors to chromatin revealed a hierarchy of protein interactions within the repair complex and suggests amplification of the damage signal. We conclude that activation of the DDR does not require DNA damage and stable association of repair factors with chromatin is likely a critical step in triggering, amplifying, and maintaining the DDR signal.
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In the citing paper
“This conclusion is in line with earlier tethering experiments demonstrating that a DNA lesion is not an obligatory part of the DDR machinery and DDR signaling can occur in its absence, allowing for the possibility of DDR initiation by stimuli other than DNA damage, such as chromatin structure (Bonilla et al., 2008; Soutoglou and Misteli, 2008).”
From Activation of DNA Damage Response Signaling by Condensed Chromatin (2014) · cites this paper as Soutoglou and Misteli, 2008
In the citing paper
“This conclusion is in line with earlier tethering experiments demonstrating that a DNA lesion is not an obligatory part of the DDR machinery and DDR signaling can occur in its absence, allowing for the possibility of DDR initiation by stimuli other than DNA damage, such as chromatin structure (Bonilla et al., 2008; Soutoglou and Misteli, 2008).”
From Activation of DNA Damage Response Signaling by Condensed Chromatin (2014) · cites this paper as Soutoglou and Misteli, 2008
In the citing paper
“No labeling by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was detected”
From Activation of DNA Damage Response Signaling by Condensed Chromatin (2014) · cites this paper as Soutoglou and Misteli, 2008
In the citing paper
“The MRN complex, MDC1, and H2AX are essential for the recruitment of ATM to the site of DSBs for efficient ATM-mediated DDR activation.”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [219]
In the citing paper
“suggesting that DDR activation requires the stable association of DNA repair proteins in HR, but not DNA damage per se [219]”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [219]
In the citing paper
“the prolonged binding to chromatin by repair proteins, such as Mre11, Nbs1 and MDC1, can elicit an ATM-dependent DDR in the absence of DNA damage”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [219]
Citations
Cites
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Positional stability of single double-strand breaks in mammalian cells
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Self-citationMDC1 is required for the intra-S-phase DNA damage checkpoint
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Mdc1 couples DNA double‐strand break recognition by Nbs1 with its H2AX‐dependent chromatin retention
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The DNA Damage Response: Making It Safe to Play with Knives
Ciccia, A., & Elledge, S. J. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.019 · Cited by 4,368
ATR: an essential regulator of genome integrity
Cimprich, K. A., & Cortez, D. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2450 · Cited by 1,798
The ATM protein kinase: regulating the cellular response to genotoxic stress, and more
Shiloh, Y., & Ziv, Y. (2013) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3546 · Cited by 1,649
-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin
Kinner, A., Wu, W., Staudt, C., & Iliakis, G. E. (2008) · Nucleic Acids Research · doi:10.1093/nar/gkn550 · Cited by 1,303
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications
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Metadata
- Authors
- Soutoglou, E., & Misteli, T.
- Affiliations
- National Institutes of Health (US)
- Venue
- Science
- Published
- 2008-06-13
- Volume
- 320
- Issue
- 5882
- Pages
- 1507-1510
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2575099
- OpenAlex
- W2067328670
- Cited by
- 299
- References
- 21
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 9 · 2023: 9 · 2022: 9 · 2021: 7 · 2020: 10 · 2019: 11 · 2018: 14 · 2017: 15 · 2016: 13 · 2015: 15 · 2014: 26 · 2013: 21 · 2012: 19
- FWCI
- 15.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (Z01BC010309)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- DNA damage response, ATM, DNA repair proteins, chromatin binding, signal amplification, protein-protein interaction
- MeSH terms
- Tumor Suppressor p53-Binding Protein 1, Checkpoint Kinase 1, MRE11 Homologue Protein, Animals, Cell Cycle, Cells, Cultured, Chromatin, Chromosomal Proteins, Non-Histone, DNA Damage, DNA Repair, DNA-Binding Proteins, Histones, Nuclear Proteins, Phosphorylation, Protein Kinases, Recombinant Fusion Proteins, Signal Transduction, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Tumor Suppressor Proteins, NIH 3T3 Cells, DNA Repair Enzymes, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Mice, Ataxia Telangiectasia Mutated Proteins, Checkpoint Kinase 2
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