Cited by 5,683DNA Repair MechanismsGenetic factors in colorectal cancerCarcinogens and Genotoxicity Assessment

DNA Repair and Mutagenesis

Friedberg, Errol C., Walker, Graham C., Siede, Wolfram, Wood, Richard D., Schultz, Roger A., Ellenberger, Tom·2005·ASM Press eBooks

Abstract

DNA damage Mutations The reversal of base damage Base excision repair Nucleotide excision repair in prokaryotes Nucleotide excision repair in lower eukaryotes Nucleotide excision repair in mammalian cells: general considerations and chromatin dynamics Nucleotide excision repair in mammalian cells: genes and proteins Mismatch repair The SOS response and recombinational repair in prokaryotes Mutagenesis in prokaryotes Mutagenesis in eukaryotes Other DNA damage tolerance responses in eukaryotes Hereditary diseases with defective responses to DNA damage

Integrity signals

Registry

Crossref · 10.1128/9781555816704

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

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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?

  • CPDs form a four-member ring involving C5 and C6 of neighboring bases, while 6-4PPs form a noncyclic bond between C6 of the 5′ end and C4 of the 3′ end via oxetane or azetidine intermediates.

    “CPDs correspond to the formation of a four-member ring structure involving C5 and C6 of both neighboring bases whereas 6-4PPs are formed by a noncyclic bond between C6 (of the 5′-end) and C4 (of the 3′-end) of the involved pyrimidines via spontaneous rearrangement of the oxetane (when the 3′-end is thymine) (Figure 3(a)) or azetidine (when the 3′-end is cytosine) (Figure 3(b)) intermediates [5, 44”
  • UV-B radiation leads to three major classes of DNA lesions: CPDs, 6-4PPs, and their Dewar isomers.

    “UV-B radiation is one of the most important energetic solar components that may lead to the formation of three major classes of DNA lesions, such as cyclobutane pyrimidine dimers (CPDs), pyrimidine 6-4 pyrimidone photoproducts (6-4PPs), and their Dewar isomers (Figure 2) [5, 22, 23, 41–43].”
  • Recombinational repair is a widespread mechanism that efficiently repairs double-strand breaks and single-strand gaps caused by ionizing radiation, UVR, ROS, and chemotherapeutic genotoxic chemicals.

    “It is one of the widespread mechanisms which efficiently repair double-strand breaks (DSBs) and single-strand gaps in damaged DNA by a series of complex biochemical reactions, as a result of ionizing radiation, UVR, ROS, and chemotherapeutic genotoxic chemicals [5].”

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Authors
Friedberg, E. C., Walker, G. C., Siede, W., Wood, R. D., Schultz, R. A., & Ellenberger, T.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Massachusetts Institute of Technology (US)
  • University of North Texas Health Science Center (US)
  • University of Pittsburgh (US)
  • Harvard University (US)
Venue
ASM Press eBooks
Publisher
ASM Press
Published
2005-11-22
OpenAlex
W1491876634
Cited by
5,683
References
0
Citations by year
2026: 20 · 2025: 48 · 2024: 59 · 2023: 87 · 2022: 81 · 2021: 131 · 2020: 114 · 2019: 128 · 2018: 125 · 2017: 110 · 2016: 147 · 2015: 147 · 2014: 207 · 2013: 225 · 2012: 219
FWCI
104.29
Type
book
Language
en
Open access
closed
Locations
ASM Press eBooks (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords
DNA repair, mutagenesis, DNA damage, base excision repair, nucleotide excision repair, DNA mismatch repair, SOS response, recombinational repair, DNA damage tolerance, chromatin dynamics, genetic disorders, prokaryotes, eukaryotes

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