Cited by 447DNA Repair MechanismsCarcinogens and Genotoxicity AssessmentGenetic factors in colorectal cancer

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Subpathways of nucleotide excision repair and their regulation

Hanawalt, Philip C·2002·Oncogene

DOI 10.1038/sj.onc.1206096

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Abstract

Nucleotide excision repair provides an important cellular defense against a large variety of structurally unrelated DNA alterations. Most of these alterations, if unrepaired, may contribute to mutagenesis, oncogenesis, and developmental abnormalities, as well as cellular lethality. There are two subpathways of nucleotide excision repair; global genomic repair (GGR) and transcription coupled repair (TCR), that is selective for the transcribed DNA strand in expressed genes. Some of the proteins involved in the recognition of DNA damage (including RNA polymerase) are also responsive to natural variations in the secondary structural features of DNA. Gratuitous repair events in undamaged DNA might then contribute to genomic instability. However, damage recognition enzymes for GGR are normally maintained at very low levels unless the cells are genomically stressed. GGR is controlled through the SOS stress response in E. coli and through the activated p53 tumor suppressor in human cells. These inducible responses in human cells are important, as they have been shown to operate upon chemical carcinogen DNA damage at levels to which humans are environmentally exposed. Interestingly, most rodent tissues are deficient in the p53-dependent GGR pathway. Since rodents are used as surrogates for environmental cancer risk assessment, it is essential that we understand how they differ from humans with respect to DNA repair and oncogenic responses to environmental genotoxins. In the case of terminally differentiated mammalian cells, a new paradigm has appeared in which GGR is attenuated but both strands of expressed genes are repaired efficiently.

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Quality Control by DNA Repair
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Authors: Hanawalt, P. C.
Affiliations: Stanford University (US)
Corresponding author: Hanawalt, Philip C
ORCID: Hanawalt, Philip C
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2002-12-16
Volume: 21
Issue: 58
Pages: 8949-8956
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1206096
OpenAlex: W1979123830
Cited by: 447
References: 62
Citations by year: 2026: 2 · 2025: 1 · 2024: 7 · 2023: 4 · 2022: 6 · 2021: 12 · 2020: 11 · 2019: 11 · 2018: 9 · 2017: 11 · 2016: 14 · 2015: 20 · 2014: 20 · 2013: 24 · 2012: 24
FWCI: 1.74
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA91456, R01CA077712, CA90915, R01CA090915, CA-44349, R35CA044349, CA-77712, R01CA091456)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
Keywords: nucleotide excision repair, transcription-coupled repair, DNA damage recognition, RNA polymerase, genomic instability, SOS response, p53, cancer risk assessment, terminally differentiated cells, mutagenesis
MeSH terms: Animals, Cell Differentiation, DNA Damage, DNA Repair, Escherichia coli, Humans, Neurons, Oncogenic Viruses, Species Specificity, Gene Expression Regulation, Bacterial, Tumor Suppressor Protein p53

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