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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.
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“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]
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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
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