ReviewFree radical biology & medicine2017
Repair of 8-oxoG:A mismatches by the MUTYH glycosylase: Mechanism, metals and medicine.
Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 101 citations in OpenAlex.
- Coordinated mitochondrial quality control underlies oxidative stress resilience in MUSE stem cells.Redox report : communications in free radical research · 2026Article
- MUTYH Activity Maintains Telomere Stability in Response to Chronic Telomeric 8-Oxoguanine Damage in Cancer Cells.Biomolecules · 2026Article
- Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.International journal of radiation biology · 2026Review
- Structural Basis for Nucleobase Activation by the Adenine DNA Glycosylase MutY.Chembiochem : a European journal of chemical biology · 2026Article
- OGG1 increases exercise endurance via elevated skeletal muscle FGF21.The Journal of biological chemistry · 2026Article
- Dynamic Landscape of Alternative Splicing During Early Embryogenesis of the Rhesus Monkey.International journal of molecular sciences · 2026Article
- Pathophysiology of reactive oxygen species (ROS).Archives of toxicology · 2026Review
- Structural Basis for Nucleobase Activation by the Adenine DNA Glycosylase MutY.bioRxiv : the preprint server for biology · 2026Article
- Germline variant spectrum of hereditary cancer susceptibility genes in a Chinese cohort.Human genomics · 2025Article
- Translesion synthesis and microhomology-mediated end-joining repair in trypanosomatids.PLoS neglected tropical diseases · 2025Review
- Saturation mapping of MUTYH variant effects using DNA repair reporters.American journal of human genetics · 2025Article
- Protein-Protein Interactions in Base Excision Repair.Biomolecules · 2025Review
- Structure of human MUTYH and functional profiling of cancer-associated variants reveal an allosteric network between its [4Fe-4S] cluster cofactor and active site required for DNA repair.Nature communications · 2025Article
- HUWE1-Mediated Degradation of MUTYH Facilitates DNA Damage and Mitochondrial Dysfunction to Promote Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- 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
- The Role of Reactive Oxygen Species in Colorectal Cancer Initiation and Progression: Perspectives on Theranostic Approaches.Cancers · 2025Review
- OGG1 and MUTYH repair activities promote telomeric 8-oxoguanine induced senescence in human fibroblasts.Nature communications · 2025Article
- The interplay of DNA damage and repair, gene expression, and mutagenesis in mammalian cells during oxidative stress.Carcinogenesis · 2024Article
- A maternal germline mutator phenotype in a family affected by heritable colorectal cancer.Genetics · 2024Article
- A maternal germline mutator phenotype in a family affected by heritable colorectal cancer.medRxiv : the preprint server for health sciences · 2024Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen and nitrogen species (RONS) may infringe on the passing of pristine genetic information by inducing DNA inter- and intra-strand crosslinks, protein-DNA crosslinks, and chemical alterations to the sugar or base moieties of DNA. 8-Oxo-7,8-dihydroguanine (8-oxoG) is one of the most prevalent DNA lesions formed by RONS and is repaired through the base excision repair (BER) pathway involving the DNA repair glycosylases OGG1 and MUTYH in eukaryotes. MUTYH removes adenine (A) from 8-oxoG:A mispairs, thus mitigating the potential of G:C to T:A transversion mutations from occurring in the genome. The paramount role of MUTYH in guarding the genome is well established in the etiology of a colorectal cancer predisposition syndrome involving variants of MUTYH, referred to as MUTYH-associated polyposis (MAP). In this review, we highlight recent advances in understanding how MUTYH structure and related function participate in the manifestation of human disease such as MAP. Here we focus on the importance of MUTYH's metal cofactor sites, including a recently discovered "Zinc linchpin" motif, as well as updates to the catalytic mechanism. Finally, we touch on the insight gleaned from studies with MAP-associated MUTYH variants and recent advances in understanding the multifaceted roles of MUTYH in the cell, both in the prevention of mutagenesis and tumorigenesis.
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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.