ArticlePloS one2010
The Mutyh base excision repair gene influences the inflammatory response in a mouse model of ulcerative colitis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- A systematic review of methylome-wide associations with anxiety disorders.Translational psychiatry · 2026Pooled it
- FSHing for DNA Damage: Key Features of MutY Detection of 8-Oxoguanine:Adenine Mismatches.Accounts of chemical research · 2024Review
- 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
- Association of Pathogenic Variants in Hereditary Cancer Genes With Multiple Diseases.JAMA oncology · 2022Article
- Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy.Biomedicines · 2022Review
- Review
- Designer Fluorescent Adenines Enable Real-Time Monitoring of MUTYH Activity.ACS central science · 2020Article
- The role of mouse models in colorectal cancer research-The need and the importance of the orthotopic models.Animal models and experimental medicine · 2020Review
- OGG1 deficiency alters the intestinal microbiome and increases intestinal inflammation in a mouse model.PloS one · 2020Article
- The MUTYH base excision repair gene protects against inflammation-associated colorectal carcinogenesis.Oncotarget · 2015Article
- Article
- What are the best routes to effectively model human colorectal cancer?Molecular oncology · 2013Review
- MUTYH DNA glycosylase: the rationale for removing undamaged bases from the DNA.Frontiers in genetics · 2013Article
- Apurinic/apyrimidinic endonuclease 1, the sensitive marker for DNA deterioration in dextran sulfate sodium-induced acute colitis.Redox report : communications in free radical research · 2013Article
- 8-Oxoguanine DNA glycosylase (OGG1) deficiency increases susceptibility to obesity and metabolic dysfunction.PloS one · 2012Article
- MUTYH-associated polyposis (MAP), the syndrome implicating base excision repair in inherited predisposition to colorectal tumors.Frontiers in oncology · 2012Article
- Interplay between DNA repair and inflammation, and the link to cancer.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Mutyh DNA glycosylase is involved in the repair of oxidized DNA bases. Mutations in the human MUTYH gene are responsible for colorectal cancer in familial adenomatous polyposis. Since defective DNA repair genes might contribute to the increased cancer risk associated with inflammatory bowel diseases, we compared the inflammatory response of wild-type and Mutyh(-/-) mice to oxidative stress. METHODOLOGY/PRINCIPAL
findingsThe severity of colitis, changes in expression of genes involved in DNA repair and inflammation, DNA 8-oxoguanine levels and microsatellite instability were analysed in colon of mice treated with dextran sulfate sodium (DSS). The Mutyh(-/-) phenotype was associated with a significant accumulation of 8-oxoguanine in colon DNA of treated mice. A single DSS cycle induced severe acute ulcerative colitis in wild-type mice, whereas lesions were modest in Mutyh(-/-) mice, and this was associated with moderate variations in the expression of several cytokines. Eight DSS cycles caused chronic colitis in both wild-type and Mutyh(-/-) mice. Lymphoid hyperplasia and a significant reduction in Foxp3(+) regulatory T cells were observed only in Mutyh(-/-) mice.
conclusionsThe findings indicate that, in this model of ulcerative colitis, Mutyh plays a major role in maintaining intestinal integrity by affecting the inflammatory response.
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