The DOI matches its Crossref record; 61 of the 62 references it cites were found in a registry or an index.
Subpathways of nucleotide excision repair and their regulation
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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“One sub-pathway of NER, global genome NER (GG-NER), removes damage from the entire genome, whereas DNA damage in the transcribed strand of active genes is preferentially eliminated by transcription-coupled NER (TC-NER) [3].”
From NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites (2013) · cites this paper as [3]
In the citing paper
“The NER pathway is subdivided into global genome repair (GG-NER) and transcription-coupled repair (TC-NER) [4].”
From Gap-filling and bypass at the replication fork are both active mechanisms for tolerance of low-dose ultraviolet-induced DNA damage in the human genome (2014) · cites this paper as [4]
Citations
Cites
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“The analysis of the repair of UV-induced cyclobutane pyrimidine dimers (CPDs) in transcriptionally active versus inactive regions of the genome, and within transcribed and non-transcribed strands of expressed genes revealed the two distinct subpathways of nucleotide excision repair: TCR and GGR (Bohr et al., 1985; Mel…”
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Self-citationMolecular Mechanism of Transcription-Repair Coupling
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Self-citation
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Cited by
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Cellular processing of platinum anticancer drugs
Wang, D., & Lippard, S. J. (2005) · Nature Reviews Drug Discovery · doi:10.1038/nrd1691 · Cited by 3,801
Molecular Mechanisms of Mammalian DNA Repair and the DNA Damage Checkpoints
Sancar, A., Lindsey-Boltz, L. A., Ünsal-Kaçmaz, K., & Linn, S. (2004) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.73.011303.073723 · Cited by 3,317
Hoeijmakers, J. H. J. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804615 · Cited by 2,239
Transcription-coupled DNA repair: two decades of progress and surprises
Hanawalt, P. C., & Spivak, G. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2549 · Cited by 1,081
Self-citationBalancing repair and tolerance of DNA damage caused by alkylating agents
Fu, D., Calvo, J. A., & Samson, L. D. (2012) · Nature reviews. Cancer · doi:10.1038/nrc3185 · Cited by 977
Metadata
- Authors
- Hanawalt, P. C.
- Affiliations
- Stanford University (US)
- Corresponding author
- Hanawalt, Philip C
- ORCID
- Hanawalt, Philip C
- Venue
- Oncogene
- Published
- 2002-12-16
- Volume
- 21
- Issue
- 58
- Pages
- 8949-8956
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- 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
- 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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