The DOI matches its Crossref record; 106 of the 106 references it cites were found in a registry or an index.
The DNA-damage response in human biology and disease
Open accessAbstract
The prime objective for every life form is to deliver its genetic material, intact and unchanged, to the next generation. This must be achieved despite constant assaults by endogenous and environmental agents on the DNA. To counter this threat, life has evolved several systems to detect DNA damage, signal its presence and mediate its repair. Such responses, which have an impact on a wide range of cellular events, are biologically significant because they prevent diverse human diseases. Our improving understanding of DNA-damage responses is providing new avenues for disease management.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These foci mark individual sites of DNA damage and contribute to checkpoint enforcement and cell cycle arrest, until damage has been repaired”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [21]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Some DDR factors accumulate at sites of DNA damage and form cytologically detectable nuclear foci composed of extended chromatin modification events, such as the phosphorylation of histone H2AX, and the proteins associated with them, including MDC1, 53BP1 and the activated form of the kinase ataxia telangiectasia mutated (ATM)21”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [21]
Experimental — accuracy not yet measuredIn the citing paper
“Two variants of canonical NHEJ pathway exist—Ku-independent NHEJ pathway microhomology-mediated end-joining (MMEJ) and alternative end-joining (AEJ)—but their activity is connected with sequence deletions [4].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [4]
In the citing paper
“The DNA damage response (DDR) pathway plays a critical role in maintaining genomic stability and preventing carcinogenesis [1].”
From NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites (2013) · cites this paper as [1]
In the citing paper
“Defects in DSB repair can result in cell cycle arrest, apoptosis or genomic aberrations and have been linked to both disease progression and a premature onset of aging phenotypes (2,3).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [2]
In the citing paper
“To maintain genome stability, the DDR pathways are conserved surveillance mechanisms coordinating DNA repair, cell cycle progression, transcription, apoptosis, and senescence [19, 39–41].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [39]
In the citing paper
“Activation of the DDR in response to DNA damage is essential for the maintenance of genome integrity [67].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [67]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy
Farmer, H., McCabe, N., Lord, C. J., Tutt, A. N. J., Johnson, D. A., Richardson, T. B., Santarosa, M., Dillon, K. J., Hickson, I., Knights, C., et al. (2005) · Nature · doi:10.1038/nature03445 · Cited by 6,683
Self-citationFree radicals, metals and antioxidants in oxidative stress-induced cancer
Valko, M., Rhodes, C. J., Moncol, J., Izakovic, M., & Mazur, M. (2006) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2005.12.009 · Cited by 6,680
Glioma stem cells promote radioresistance by preferential activation of the DNA damage response
Bao, S., Wu, Q., McLendon, R. E., Hao, Y., Shi, Q., Hjelmeland, A. B., Dewhirst, M. W., Bigner, D. D., & Rich, J. N. (2006) · Nature · doi:10.1038/nature05236 · Cited by 6,363
Friedberg, E. C., Walker, G. C., Siede, W., Wood, R. D., Schultz, R. A., & Ellenberger, T. (2005) · doi:10.1128/9781555816704 · Cited by 5,683
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
Bryant, H. E., Schultz, N., Thomas, H. D., Parker, K. M., Flower, D., Lopez, E., Kyle, S., Meuth, M., Curtin, N. J., & Helleday, T. (2005) · Nature · doi:10.1038/nature03443 · Cited by 5,198
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Genetic instabilities in human cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1998) · Nature · doi:10.1038/25292 · Cited by 4,168 · cited 1×
“Furthermore, chromosomal instability is seen in most sporadic solid tumours 61 .”
BackgroundGenome maintenance mechanisms for preventing cancer
Hoeijmakers, J. H. J. (2001) · Nature · doi:10.1038/35077232 · Cited by 3,939
The Causes of Cancer: Quantitative Estimates of Avoidable Risks of Cancer in the United States Today
Doll, R., & Peto, R. (1981) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/66.6.1192 · Cited by 3,927 · cited 1×
“Today, probably themost prevalent environmental cancer-causing chemicals are those produced by tobacco products, which trigger various cancers, most notably those of the lung, oral cavity and adjacent tissues 6,7 .”
BackgroundStratton, M. R., Campbell, P. J., & Futreal, P. A. (2009) · Nature · doi:10.1038/nature07943 · Cited by 3,625
Cited by
Sorted by citations
Hallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590
Reactive oxygen species (ROS) as pleiotropic physiological signalling agents
Sies, H., & Jones, D. P. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0230-3 · Cited by 5,335
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
Analysis of 100,000 human cancer genomes reveals the landscape of tumor mutational burden
Chalmers, Z. R., Connelly, C. F., Fabrizio, D., Gay, L., Ali, S. M., Ennis, R., Schrock, A., Campbell, B., Shlien, A., Chmielecki, J., et al. (2017) · Genome Medicine · doi:10.1186/s13073-017-0424-2 · Cited by 3,519
Cellular senescence in ageing: from mechanisms to therapeutic opportunities
Di Micco, R., Krizhanovsky, V., Baker, D., & d’Adda di Fagagna, F. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-00314-w · Cited by 2,277
Metadata
- Authors
- Jackson, S. P., & Bartek, J.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Jackson, Stephen P.
- ORCID
- Jackson, Stephen P.
- Venue
- Nature
- Published
- 2009-10-22
- Volume
- 461
- Issue
- 7267
- Pages
- 1071-1078
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2906700
- OpenAlex
- W2145200068
- Cited by
- 6,092
- References
- 106
- Citations by year
- 2026: 344 · 2025: 369 · 2024: 417 · 2023: 469 · 2022: 489 · 2021: 511 · 2020: 448 · 2019: 416 · 2018: 344 · 2017: 402 · 2016: 381 · 2015: 338 · 2014: 310 · 2013: 279 · 2012: 241
- FWCI
- 14.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Foundation for Cancer Research
- Wellcome Trust
- Cancer Research UK (A5290)
- European Commission
- Danmarks Grundforskningsfond
- Dansk Kræftforsknings Fond
- Biotechnology and Biological Sciences Research Council
- 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
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- DNA damage response, DNA repair, DNA damage detection, ionizing radiation, environmental chemicals, endogenous DNA damage, signal transduction, disease prevention, genotoxicity
- MeSH terms
- Cell Cycle, Disease, DNA Damage, DNA Repair, Humans, Signal Transduction, Genome, Human
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
