ArticleDNA repair2015
Distinct functional consequences of MUTYH variants associated with colorectal cancer: Damaged DNA affinity, glycosylase activity and interaction with PCNA and Hus1.
Article in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Regulatory networks of iron sulfur cluster biology in cancer mechanisms and therapeutic perspectives.iScience · 2026Review
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 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
- Cellular Repair of Synthetic Analogs of Oxidative DNA Damage Reveals a Key Structure-Activity Relationship of the Cancer-Associated MUTYH DNA Repair Glycosylase.ACS central science · 2024Article
- Germline MUTYH mutations and high-grade gliomas: Novel evidence for a potential association.Genes, chromosomes & cancer · 2022Article
- Noncatalytic Domains in DNA Glycosylases.International journal of molecular sciences · 2022Review
- MUTYH: Not just polyposis.World journal of clinical oncology · 2020Review
- 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
- Single molecule glycosylase studies with engineered 8-oxoguanine DNA damage sites show functional defects of a MUTYH polyposis variant.Nucleic acids research · 2019Article
- Effective Distance for DNA-Mediated Charge Transport between Repair Proteins.ACS central science · 2019Article
- Correlations of PCNA expression with thyroid cancer ultrasound and histopathologic features.International journal of clinical and experimental pathology · 2019Article
- The Zinc Linchpin Motif in the DNA Repair Glycosylase MUTYH: Identifying the ZnJournal of the American Chemical Society · 2018Article
- Iron-sulfur cluster biosynthesis and trafficking - impact on human disease conditions.Metallomics : integrated biometal science · 2018Review
- Cellular Assays for Studying the Fe-S Cluster Containing Base Excision Repair Glycosylase MUTYH and Homologs.Methods in enzymology · 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
- Oxidative Stress-Induced Protein Damage Inhibits DNA Repair and Determines Mutation Risk and Therapeutic Efficacy.Molecular cancer research : MCR · 2016Article
- The current state of eukaryotic DNA base damage and repair.Nucleic acids research · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
MUTYH is a base excision repair (BER) enzyme that prevents mutations in DNA associated with 8-oxoguanine (OG) by catalyzing the removal of adenine from inappropriately formed OG:A base-pairs. Germline mutations in the MUTYH gene are linked to colorectal polyposis and a high risk of colorectal cancer, a syndrome referred to as MUTYH-associated polyposis (MAP). There are over 300 different MUTYH mutations associated with MAP and a large fraction of these gene changes code for missense MUTYH variants. Herein, the adenine glycosylase activity, mismatch recognition properties, and interaction with relevant protein partners of human MUTYH and five MAP variants (R295C, P281L, Q324H, P502L, and R520Q) were examined. P281L MUTYH was found to be severely compromised both in DNA binding and base excision activity, consistent with the location of this variation in the iron-sulfur cluster (FCL) DNA binding motif of MUTYH. Both R295C and R520Q MUTYH were found to have low fractions of active enzyme, compromised affinity for damaged DNA, and reduced rates for adenine excision. In contrast, both Q324H and P502L MUTYH function relatively similarly to WT MUTYH in both binding and glycosylase assays. However, P502L and R520Q exhibited reduced affinity for PCNA (proliferation cell nuclear antigen), consistent with their location in the PCNA-binding motif of MUTYH. Whereas, only Q324H, and not R295C, was found to have reduced affinity for Hus1 of the Rad9-Hus1-Rad1 complex, despite both being localized to the same region implicated for interaction with Hus1. These results underscore the diversity of functional consequences due to MUTYH variants that may impact the progression of MAP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.