ArticleProceedings of the National Academy of Sciences of the United States of America2025
OGG1 augments the transcriptional activation of
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Navigating the base excision repair pathway in chromatin-focus on oxidative DNA damage.Nucleic acids research · 2026Review
- An Integrated DNA Nanoprobe for Intranuclear Imaging and In Situ Profiling of OGG1 Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epigenetic consequences of DNA damage.Molecular cell · 2026Review
- Lacticaseibacillus rhamnosus LRa05 mitigates DSS-Induced colitis via boosting beneficial gut microbiota and facilitating CD4⁺Foxp3⁺ Treg differentiation.BMC microbiology · 2026Article
- Regulatory T cells in breast cancer drivers of immune suppression and targets for immunotherapy.Frontiers in immunology · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Dynamic genome-wide mapping reveals how chromatin context shapes OGG1-mediated repair and related mutagenesis in human cells.Nucleic acids research · 2025Article
- OGG1 augments the transcriptional activation ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
8-oxo-7,8-dihydroguanine (8-oxoG), the most frequent form of oxidative-DNA-base lesion caused by ROS, is recognized and repaired by 8-oxoguanine DNA glycosylase 1 (OGG1) through base excision repair (BER) pathway. Beyond its role in DNA repair, OGG1 has been shown to promote transcriptional activation of proinflammatory mediators and contribute to both acute and chronic lung inflammation. However, pioneering studies have shown an anti-inflammation role for OGG1 in inflammatory bowel disease (IBD), but its underlying molecular mechanism remains unclear. In the present study, we unveiled that OGG1 plays an important role in the differentiation of inducible regulatory T cells (iTregs). Binding of OGG1 to 8-oxoG facilitated the recruitment of Smad3 to the
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