ArticleEnvironmental and molecular mutagenesis2020
Enhancing the sensitivity of the thymidine kinase assay by using DNA repair-deficient human TK6 cells.
Article in Environmental and molecular mutagenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- REV7 associates with ATRIP and inhibits ATR kinase activity.Nucleic acids research · 2026Article
- Dual-directional epi-genotoxicity assay for assessing chemically induced epigenetic effects utilizing the housekeeping TK gene.Scientific reports · 2025Article
- Comprehensive whole-genome sequencing reveals origins of mutational signatures associated with aging, mismatch repair deficiency and temozolomide chemotherapy.Nucleic acids research · 2025Article
- REV7-p53 interaction inhibits ATM-mediated DNA damage signaling.Cell cycle (Georgetown, Tex.) · 2024Article
- Enhancing the sensitivity of the thymidine kinase assay by using DNA repair-deficient human TK6 cells.Environmental and molecular mutagenesis · 2020Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The OECD guidelines define the bioassays of identifying mutagenic chemicals, including the thymidine kinase (TK) assay, which specifically detects the mutations that inactivate the TK gene in the human TK6 lymphoid line. However, the sensitivity of this assay is limited because it detects mutations occurring only in the TK gene but not any other genes. Moreover, the limited sensitivity of the conventional TK assay is caused by the usage of DNA repair-proficient wild-type cells, which are capable of accurately repairing DNA damage induced by chemicals. Mutagenic chemicals produce a variety of DNA lesions, including base lesions, sugar damage, crosslinks, and strand breaks. Base damage causes point mutations and is repaired by the base excision repair (BER) and nucleotide excision repair (NER) pathways. To increase the sensitivity of TK assay, we simultaneously disrupted two genes encoding XRCC1, an important BER factor, and XPA, which is essential for NER, generating XRCC1
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