The DOI matches its Crossref record; 274 of the 280 references it cites were found in a registry or an index.
DNA repair mechanisms in dividing and non-dividing cells
Open accessAbstract
DNA damage created by endogenous or exogenous genotoxic agents can exist in multiple forms, and if allowed to persist, can promote genome instability and directly lead to various human diseases, particularly cancer, neurological abnormalities, immunodeficiency and premature aging. To avoid such deleterious outcomes, cells have evolved an array of DNA repair pathways, which carry out what is typically a multiple-step process to resolve specific DNA lesions and maintain genome integrity. To fully appreciate the biological contributions of the different DNA repair systems, one must keep in mind the cellular context within which they operate. For example, the human body is composed of non-dividing and dividing cell types, including, in the brain, neurons and glial cells. We describe herein the molecular mechanisms of the different DNA repair pathways, and review their roles in non-dividing and dividing cells, with an eye toward how these pathways may regulate the development of neurological disease.
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 cited source says what the claim attributes to it.
In the citing paper
“Although a certain level of homology-directed repair has been observed in non-dividing cells, such as neurons [52], other DNA repair pathways than homologous recombination are more active in these long-lived postmitotic cells [53].”
From Circumventing the packaging limit of AAV-mediated gene replacement therapy for neurological disorders (2022) · cites this paper as [53]
In the citing paper
“For CSB, it is already known that it can interact with several members of BER pathway, including the strandbreak response protein poly(ADP-ribose) polymerase-1 (PARP1), endonuclease VIII-like 1 (NEIL1) DNA glycosylase, and APE1 [227].”
From Sunlight damage to cellular DNA: focus on oxidatively generated lesions (2017) · cites this paper as [227]
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
2 retracted
Fousteri, M., Vermeulen, W., van Zeeland, A. A., & Mullenders, L. H. F. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.06.029 · Cited by 387
RetractedMoser, J., Kool, H., Giakzidis, I., Caldecott, K., Mullenders, L. H. F., & Fousteri, M. I. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.06.014 · Cited by 261
RetractedThe DNA-damage response in human biology and disease
Jackson, S. P., & Bartek, J. (2009) · Nature · doi:10.1038/nature08467 · Cited by 6,092
Instability and decay of the primary structure of DNA
Lindahl, T. (1993) · Nature · doi:10.1038/362709a0 · Cited by 5,679
Genome maintenance mechanisms for preventing cancer
Hoeijmakers, J. H. J. (2001) · Nature · doi:10.1038/35077232 · Cited by 3,939
The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway
Lieber, M. R. (2010) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.052308.093131 · Cited by 2,882
Hoeijmakers, J. H. J. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804615 · Cited by 2,239
Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG
Shibutani, S., Takeshita, M., & Grollman, A. P. (1991) · Nature · doi:10.1038/349431a0 · Cited by 2,224
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
Double-Strand Break End Resection and Repair Pathway Choice
Symington, L. S., & Gautier, J. (2011) · Annual Review of Genetics · doi:10.1146/annurev-genet-110410-132435 · Cited by 1,556
Research works printed but not linked: 1
- Clements, 2004, The ataxia-oculomotor apraxia 1 gene product has a role distinct from ATM and interacts with the DNA strand break repair proteins XRCC1 and XRCC4, DNA Repair (Amst), 3, 1493, 10.1016/j.dnarep.2004.06.017 · DOI
Cited by
Sorted by citations
Huang, R., & Zhou, P. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00648-7 · Cited by 1,015
Oxidative stress and male infertility
Bisht, S., Faiq, M. A., Tolahunase, M., & Dada, R. (2017) · Nature Reviews Urology · doi:10.1038/nrurol.2017.69 · Cited by 918
MutationalPatterns: comprehensive genome-wide analysis of mutational processes
Blokzijl, F., Janssen, R., van Boxtel, R., & Cuppen, E. (2018) · Genome Medicine · doi:10.1186/s13073-018-0539-0 · Cited by 660
DNA damage and its links to neurodegeneration
Madabhushi, R., Pan, L., & Tsai, L.-H. (2014) · Neuron · doi:10.1016/j.neuron.2014.06.034 · Cited by 654
NAD(+) in aging: molecular mechanisms and translational implications
Fang, E. F., Lautrup, S., Hou, Y., Demarest, T. G., Croteau, D. L., Mattson, M. P., & Bohr, V. A. (2017) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2017.08.001 · Cited by 501
Metadata
- Authors
- Iyama, T., & Wilson, D. M.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Wilson, David M.
- ORCID
- Wilson, David M.
- Venue
- DNA Repair
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 12
- Issue
- 8
- Pages
- 620-636
- ISSN
- 1568-7856 (ISSN-L)
- 1568-7864
- PMC
- PMC3720834
- OpenAlex
- W2004257622
- Cited by
- 697
- References
- 280
- Citations by year
- 2026: 20 · 2025: 37 · 2024: 49 · 2023: 56 · 2022: 43 · 2021: 69 · 2020: 58 · 2019: 59 · 2018: 65 · 2017: 57 · 2016: 72 · 2015: 62 · 2014: 47 · 2013: 2
- FWCI
- 27.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- DNA repair (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (ZIAAG000751)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- DNA repair pathways, genome stability, genetic damage, dividing cells, non-dividing cells, neurons, glial cells, neurological disorders, cancer, premature aging, immunodeficiency, DNA lesions
- MeSH terms
- Animals, Disease Models, Animal, DNA, DNA Damage, DNA Repair, Humans, Neurons, Pyrimidine Dimers, O(6)-Methylguanine-DNA Methyltransferase
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
