Cited by 51DNA Repair MechanismsPARP inhibition in cancer therapyCRISPR and Genetic Engineering

Polymerases in nonhomologous end joining: Building a bridge over broken chromosomes

Open access
Ramsden, Dale A.·2011·Antioxidants & Redox Signaling

Abstract

Repair of double-strand breaks in chromosomal DNA is essential. Unfortunately, a paradigm central to most DNA repair pathways--damaged DNA is replaced by polymerases, by using an intact, undamaged complementary strand as a template--no longer works. The nonhomologous end joining (NHEJ) pathway nevertheless still uses DNA polymerases to help repair double-strand breaks. Bacteria use a member of the archaeo-eukaryal primase superfamily, whereas eukaryotes use multiple members of the polymerase X family. These polymerases can, depending on the biologic context, accurately replace break-associated damage, mitigate loss of flanking DNA, or diversify products of repair. Polymerases specifically implicated in NHEJ are uniquely effective in these roles: relative to canonic polymerases, NHEJ polymerases have been engineered to do more with less.

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Crossref · 10.1089/ars.2010.3429

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Authors
Ramsden, D. A.
Affiliations
University of North Carolina at Chapel Hill (US)
Corresponding author
Ramsden, Dale A.
Venue
Antioxidants & Redox Signaling
Published
2011-06
Volume
14
Issue
12
Pages
2509-2519
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
OpenAlex
W2024164424
Cited by
51
References
110
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 4 · 2020: 5 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 3 · 2013: 7 · 2012: 6
FWCI
0.50
Type
journal article
Language
en
Open access
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
  • UNC Libraries
Funders
  • Leukemia and Lymphoma Society
  • National Cancer Institute (U01CA097096, CA-97096, R01CA097096)
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 › CRISPR and Genetic Engineering
Keywords
non-homologous end joining, DNA polymerase, DNA double-strand break repair, DNA end joining, bacterial DNA repair, eukaryotic DNA repair
MeSH terms
Animals, DNA, DNA-Directed DNA Polymerase, DNA Repair, Recombination, Genetic, DNA Breaks, Double-Stranded

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