ArticleDNA repair2014
Mammalian MutY homolog (MYH or MUTYH) protects cells from oxidative DNA damage.
Article in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
22 citing papers in PubMed, 37 citations in OpenAlex.
- Action-at-a-distance mutations by 8-oxo-7,8-dihydroguanine: adenine pair triggered by MUTYH.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Article
- Identification of 17 novel epigenetic biomarkers associated with anxiety disorders using differential methylation analysis followed by machine learning-based validation.Clinical epigenetics · 2025Article
- Mechanically-adaptive, resveratrol-eluting neural probes for improved intracortical recording performance and stability.Npj flexible electronics · 2025Article
- Gallium Uncouples Iron Metabolism to Enhance Glioblastoma Radiosensitivity.International journal of molecular sciences · 2024Article
- Article
- MYH16 upregulation is associated with lung adenocarcinoma aggressiveness and immune infiltration.Journal of biochemical and molecular toxicology · 2023Article
- Mammalian MutY Homolog (MYH or MUTYH) is Critical for Telomere Integrity under Oxidative Stress.OBM geriatrics · 2022Article
- Article
- The Similarities between Human Mitochondria and Bacteria in the Context of Structure, Genome, and Base Excision Repair System.Molecules (Basel, Switzerland) · 2020Review
- The DNA repair enzyme MUTYH potentiates cytotoxicity of the alkylating agent MNNG by interacting with abasic sites.The Journal of biological chemistry · 2020Article
- DNA lesions and repair in trypanosomatids infection.Genetics and molecular biology · 2020Article
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- Chk1 inhibition as a novel therapeutic strategy in melanoma.Oncotarget · 2018Article
- MutY-Homolog (MYH) inhibition reduces pancreatic cancer cell growth and increases chemosensitivity.Oncotarget · 2017Article
- Association of monoallelic MUTYH mutation among Egyptian patients with colorectal cancer.Familial cancer · 2017Article
- Exome-wide single-base substitutions in tissues and derived cell lines of the constitutive Fhit knockout mouse.Cancer science · 2016Article
- Association of the Rad9-Rad1-Hus1 checkpoint clamp with MYH DNA glycosylase and DNA.DNA repair · 2015Article
- SIRT6 protein deacetylase interacts with MYH DNA glycosylase, APE1 endonuclease, and Rad9-Rad1-Hus1 checkpoint clamp.BMC molecular biology · 2015Article
- Article
- Regulation of human MutYH DNA glycosylase by the E3 ubiquitin ligase mule.The Journal of biological chemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
MutY DNA glycosylase homologs (MYH or MUTYH) reduce G:C to T:A mutations by removing misincorporated adenines or 2-hydroxyadenines paired with guanine or 8-oxo-7,8-dihydroguanine (8-oxo-G). Mutations in the human MYH (hMYH) gene are associated with the colorectal cancer predisposition syndrome MYH-associated polyposis. To examine the function of MYH in human cells, we regulated MYH gene expression by knockdown or overproduction. MYH knockdown human HeLa cells are more sensitive to the killing effects of H2O2 than the control cells. In addition, hMYH knockdown cells have altered cell morphology, display enhanced susceptibility to apoptosis, and have altered DNA signaling activation in response to oxidative stress. The cell cycle progression of hMYH knockdown cells is also different from that of the control cells following oxidative stress. Moreover, hMYH knockdown cells contain higher levels of 8-oxo-G lesions than the control cells following H2O2 treatment. Although MYH does not directly remove 8-oxo-G, MYH may generate favorable substrates for other repair enzymes. Overexpression of mouse Myh (mMyh) in human mismatch repair defective HCT15 cells makes the cells more resistant to killing and refractory to apoptosis by oxidative stress than the cells transfected with vector. In conclusion, MYH is a vital DNA repair enzyme that protects cells from oxidative DNA damage and is critical for a proper cellular response to DNA damage.
Indexed as
Identifiers
What OpenQuestion holds
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.