ArticleNucleic acids research2004
MUTYH prevents OGG1 or APEX1 from inappropriately processing its substrate or reaction product with its C-terminal domain.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- Mammalian MutY Homolog (MYH or MUTYH) is Critical for Telomere Integrity under Oxidative Stress.OBM geriatrics · 2022Article
- Structure of the mammalian adenine DNA glycosylase MUTYH: insights into the base excision repair pathway and cancer.Nucleic acids research · 2021Article
- Review
- The DNA repair enzyme MUTYH potentiates cytotoxicity of the alkylating agent MNNG by interacting with abasic sites.The Journal of biological chemistry · 2020Article
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- Single molecule glycosylase studies with engineered 8-oxoguanine DNA damage sites show functional defects of a MUTYH polyposis variant.Nucleic acids research · 2019Article
- MutY-Homolog (MYH) inhibition reduces pancreatic cancer cell growth and increases chemosensitivity.Oncotarget · 2017Article
- Impact of Ribonucleotide Backbone on Translesion Synthesis and Repair of 7,8-Dihydro-8-oxoguanine.The Journal of biological chemistry · 2016Article
- The current state of eukaryotic DNA base damage and repair.Nucleic acids research · 2015Review
- Abnormality in Wnt signaling is causatively associated with oxidative stress-induced intestinal tumorigenesis in MUTYH-null mice.International journal of biological sciences · 2014Article
- Article
- Understanding the role of the Q338H MUTYH variant in oxidative damage repair.Nucleic acids research · 2013Article
- MUTYH DNA glycosylase: the rationale for removing undamaged bases from the DNA.Frontiers in genetics · 2013Article
- Recent advances in the structural mechanisms of DNA glycosylases.Biochimica et biophysica acta · 2013Review
- Therapeutic effects of hydrogen in animal models of Parkinson's disease.Parkinson's disease · 2011Article
- Two distinct pathways of cell death triggered by oxidative damage to nuclear and mitochondrial DNAs.The EMBO journal · 2008Article
- Base-excision repair of oxidative DNA damage.Nature · 2007Review
- A genome-wide distribution of 8-oxoguanine correlates with the preferred regions for recombination and single nucleotide polymorphism in the human genome.Genome research · 2006Article
- 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.Nucleic acids research · 2005Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MutY homolog (MUTYH) excises adenine opposite 8-oxoguanine (8-oxoG) in DNA, thus preventing occurrence of G:C to T:A transversion. In cell-free extract prepared from the thymocytes of wild type but not MUTYH-null mice, adenine opposite 8-oxoG in DNA was excised by MUTYH, however, the generated apurinic (AP) site opposite 8-oxoG mostly remained unincised. Recombinant mouse MUTYH (mMUTYH) efficiently excised adenine opposite 8-oxoG and prevented mouse AP endonuclease (mAPEX1) from incising the generated AP site. In contrast, an AP site opposite 8-oxoG created by uracil DNA glycosylase or tetrahydrofuran opposite 8-oxoG was efficiently incised by mAPEX1 in the presence of an excess amount of mMUTYH. Mutant mMUTYH with R361A or G365D substitution, excised adenine opposite 8-oxoG as efficiently as did wild-type mMUTYH, but failed to prevent mAPEX1 from incising the generated AP site. Wild-type mMUTYH bound duplex oligonucleotides containing A:8-oxoG pair with a lower apparent K(d) than that of the mutants, and prevented OGG1 from excising 8-oxoG opposite adenine or the generated AP site. The G365D mutant failed to prevent OGG1 from excising 8-oxoG opposite the generated AP site, thus indicating that the protection of its own product by mMUTYH is an intrinsic function which depends on the C-terminal domain of mMUTYH.
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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.