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DNA repair in an active gene: Removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall
Abstract
DNA repair was measured in the dihydrofolate reductase gene in Chinese hamster ovary cells, amplified for the gene, by quantitating pyrimidine dimers with a specific UV-endonuclease. More than two thirds of the dimers had been removed from a 14.1 kb restriction fragment of the gene by 26 hr after irradiation (20 J/m2), while little removal was detected in fragments upstream of the gene and only 15% were removed from the genome overall. This suggests that damage processing can vary according to function or activity of affected sequences, which has general implications for correlations of DNA repair with survival and mutagenesis. Perhaps preferential repair of vital sequences facilitates UV-resistance of these cells despite low overall repair levels.
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“XPA is an indispensable factor both for transcription-coupled NER and global genome NER [7], [8].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [7]
In the citing paper
“Two subpathways of NER exist: transcription-blocking lesions in the transcribed strand (TS) of active genes are repaired quickly by transcription-coupled NER (TC-NER), whereas the rest of the genome, including the nontranscribed strand (NTS) of active genes, is repaired more slowly by global genome NER (GG-NER) (8, 33, 34, 44, 54).”
From A Role for Checkpoint Kinase-Dependent Rad26 Phosphorylation in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae (2010) · cites this paper as [8]
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LIu, S., Tseng, J.-N., Shiuan, D., & Hanawalt, P. (1997) · Molecular and General Genetics MGG · doi:10.1007/s004380050517 · Cited by 5
“Gene expression has been shown to in¯uence the e ciency of DNA repair and mutagenesis (Bohr et al. 1985; Mellon et al. 1987; Mellon and Hanawalt 1989; Oller et al. 1992).”
Background
Metadata
- Authors
- Bohr, V
- Affiliations
- Stanford University (US)
- Corresponding author
- Bohr, V
- ORCID
- Bohr, V
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1985-02
- Volume
- 40
- Issue
- 2
- Pages
- 359-369
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W1984353960
- Cited by
- 1,237
- References
- 34
- Citations by year
- 2026: 11 · 2025: 17 · 2024: 15 · 2023: 14 · 2022: 12 · 2021: 17 · 2020: 18 · 2019: 11 · 2018: 18 · 2017: 13 · 2016: 23 · 2015: 9 · 2014: 24 · 2013: 24 · 2012: 22
- FWCI
- 15.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (GM 09901)
- 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 › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- DNA repair, pyrimidine dimers, dihydrofolate reductase gene, UV-induced DNA damage, UV endonuclease, UV resistance, CHO cells, mutagenesis, cell survival
- MeSH terms
- Animals, Base Sequence, Cell Line, Cell Survival, Cricetulus, DNA Repair, Endodeoxyribonucleases, Female, Cricetinae, Multienzyme Complexes, N-Glycosyl Hydrolases, Pyrimidine Dimers, Tetrahydrofolate Dehydrogenase
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