DNA Repair and Mutagenesis
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
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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”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [5]
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].”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [5]
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].”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [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)
- ORCID
- Walker, Graham C.
- 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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