ArticleNucleic acids research2005
Functional characterization of two human MutY homolog (hMYH) missense mutations (R227W and V232F) that lie within the putative hMSH6 binding domain and are associated with hMYH polyposis.
Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 65 citations in OpenAlex.
- Client recruitment mechanism of the cytosolic Fe-S cluster assembly targeting complex.The EMBO journal · 2026Article
- 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
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- Contribution of New Adenomatous Polyposis Predisposition Genes in an Unexplained Attenuated Spanish Cohort by Multigene Panel Testing.Scientific reports · 2019Article
- A human MUTYH variant linking colonic polyposis to redox degradation of the [4Fe4S]Nature chemistry · 2018Article
- Fe-S Clusters and MutY Base Excision Repair Glycosylases: Purification, Kinetics, and DNA Affinity Measurements.Methods in enzymology · 2018Article
- Repair of 8-oxoG:A mismatches by the MUTYH glycosylase: Mechanism, metals and medicine.Free radical biology & medicine · 2017Review
- Functional Complementation Assay for 47 MUTYH Variants in a MutY-Disrupted Escherichia coli Strain.Human mutation · 2015Article
- MUTYH, an adenine DNA glycosylase, mediates p53 tumor suppression via PARP-dependent cell death.Oncogenesis · 2014Article
- Clinical evaluation of a multiple-gene sequencing panel for hereditary cancer risk assessment.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014Article
- MUTYH-associated colorectal cancer and adenomatous polyposis.Surgery today · 2014Review
- Impaired 8-hydroxyguanine repair activity of MUTYH variant p.Arg109Trp found in a Japanese patient with early-onset colorectal cancer.Oxidative medicine and cellular longevity · 2014Article
- Postreplicative mismatch repair.Cold Spring Harbor perspectives in biology · 2013Review
- Understanding the role of the Q338H MUTYH variant in oxidative damage repair.Nucleic acids research · 2013Article
- Base excision repair and cancer.Cancer letters · 2012Review
- Impaired suppressive activities of human MUTYH variant proteins against oxidative mutagenesis.World journal of gastroenterology · 2012Article
- MUTYH-associated polyposis (MAP), the syndrome implicating base excision repair in inherited predisposition to colorectal tumors.Frontiers in oncology · 2012Article
- Mutants of the base excision repair glycosylase, endonuclease III: DNA charge transport as a first step in lesion detection.Biochemistry · 2011Article
- Adenine DNA glycosylase activity of 14 human MutY homolog (MUTYH) variant proteins found in patients with colorectal polyposis and cancer.Human mutation · 2010Article
- A structural hinge in eukaryotic MutY homologues mediates catalytic activity and Rad9-Rad1-Hus1 checkpoint complex interactions.Journal of molecular biology · 2010Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
The base excision repair DNA glycosylase MutY homolog (MYH) is responsible for removing adenines misincorporated into DNA opposite guanine or 7,8-dihydro-8-oxo-guanine (8-oxoG), thereby preventing G:C to T:A mutations. Biallelic germline mutations in the human MYH gene predispose individuals to multiple colorectal adenomas and carcinoma. We have recently demonstrated that hMYH interacts with the mismatch repair protein hMSH6, and that the hMSH2/hMSH6 (hMutSalpha) heterodimer stimulates hMYH activity. Here, we characterize the functional effect of two missense mutations (R227W and V232F) associated with hMYH polyposis that lie within, or adjacent to, the putative hMSH6 binding domain. Neither missense mutation affects the physical interaction between hMYH and hMSH6. However, hMYH(R227W) has a severe defect in A/8-oxoG binding and glycosylase activities, while hMYH(V232F) has reduced A/8-oxoG binding and glycosylase activities. The glycosylase activity of the V232F mutant can be partially stimulated by hMutSalpha but cannot be restored to the wild-type level. Both mutants also fail to complement mutY-deficiency in Escherichia coli. These data define the pathogenic mechanisms underlying two further hMYH polyposis-associated mutations.
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