ArticleNucleic acids research2013
Understanding the role of the Q338H MUTYH variant in oxidative damage repair.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- MUTYH Cancer-Associated Variants Within the Interdomain Connector Differentially Impact Glycosylase Activity and Cellular DNA Repair.Chembiochem : a European journal of chemical biology · 2026Article
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- Precision genome editing and in-cell measurements of oxidative DNA damage repair enable functional and mechanistic characterization of cancer-associated MUTYH variants.Nucleic acids research · 2025Article
- Mammalian MutY Homolog (MYH or MUTYH) is Critical for Telomere Integrity under Oxidative Stress.OBM geriatrics · 2022Article
- Predictive value of genetic variants XRCC1 rs1799782, APEX1 rs1760944, and MUTYH rs3219489 for adjuvant concurrent chemoradiotherapy outcomes in oral squamous cell carcinoma patients.The pharmacogenomics journal · 2020Article
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- The Zinc Linchpin Motif in the DNA Repair Glycosylase MUTYH: Identifying the ZnJournal of the American Chemical Society · 2018Article
- Cellular Assays for Studying the Fe-S Cluster Containing Base Excision Repair Glycosylase MUTYH and Homologs.Methods in enzymology · 2018Article
- A Specific Mutational Signature Associated with DNA 8-Oxoguanine Persistence in MUTYH-defective Colorectal Cancer.EBioMedicine · 2017Article
- Repair of 8-oxoG:A mismatches by the MUTYH glycosylase: Mechanism, metals and medicine.Free radical biology & medicine · 2017Review
- Oxidized dNTPs and the OGG1 and MUTYH DNA glycosylases combine to induce CAG/CTG repeat instability.Nucleic acids research · 2016Article
- Formation and Repair of Mismatches Containing Ribonucleotides and Oxidized Bases at Repeated DNA Sequences.The Journal of biological chemistry · 2015Article
- Article
- Functional Complementation Assay for 47 MUTYH Variants in a MutY-Disrupted Escherichia coli Strain.Human mutation · 2015Article
- SIRT6 protein deacetylase interacts with MYH DNA glycosylase, APE1 endonuclease, and Rad9-Rad1-Hus1 checkpoint clamp.BMC molecular biology · 2015Article
- Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MUTYH DNA-glycosylase is indirectly engaged in the repair of the miscoding 7,8-dihydro-8-oxo-2'-deoxyguanine (8-oxodG) lesion by removing adenine erroneously incorporated opposite the oxidized purine. Inherited biallelic mutations in the MUTYH gene are responsible for a recessive syndrome, the MUTYH-associated polyposis (MAP), which confers an increased risk of colorectal cancer. In this study, we functionally characterized the Q338H variant using recombinant proteins, as well as cell-based assays. This is a common variant among human colorectal cancer genes, which is generally considered, unrelated to the MAP phenotype but recently indicated as a low-penetrance allele. We demonstrate that the Q338H variant retains a wild-type DNA-glycosylase activity in vitro, but it shows a reduced ability to interact with the replication sensor RAD9:RAD1:HUS1 (9-1-1) complex. In comparison with Mutyh(-)(/)(-) mouse embryo fibroblasts expressing a wild-type MUTYH cDNA, the expression of Q338H variant was associated with increased levels of DNA 8-oxodG, hypersensitivity to oxidant and accumulation of the population in the S phase of the cell cycle. Thus, an inefficient interaction of MUTYH with the 9-1-1 complex leads to a repair-defective phenotype, indicating that a proper communication between MUTYH enzymatic function and the S phase checkpoint is needed for effective repair of oxidative damage.
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