Cited by 698DNA Repair MechanismsPARP inhibition in cancer therapyDNA and Nucleic Acid Chemistry

DNA repair mechanisms in dividing and non-dividing cells

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Iyama, Teruaki, Wilson, David M.·2013·DNA Repair

Abstract

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.

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Crossref · 10.1016/j.dnarep.2013.04.015

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  • Although some homology-directed repair has been observed in non-dividing cells such as neurons, other DNA repair pathways than homologous recombination are more active in these long-lived postmitotic cells.

    “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].”
  • CSB can interact with several members of the BER pathway, including PARP1, NEIL1 DNA glycosylase, and APE1.

    “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].”

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  1. [153]Clements PM Breslin C Deeks ED Byrd PJ Ju L Bieganowski P Brenner C Moreira MC Taylor AM Caldecott KW 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 2004 1493 1502 15380105

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Authors
Iyama, T., & Wilson, D. M.
Affiliations
National Institutes of Health (US)
Corresponding author
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
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
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

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