ArticleNucleic acids research2012
Germline ablation of SMUG1 DNA glycosylase causes loss of 5-hydroxymethyluracil- and UNG-backup uracil-excision activities and increases cancer predisposition of Ung-/-Msh2-/- mice.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 106 citations in OpenAlex.
- Structural basis for uracil removal from DNA by human SMUG1.Nature communications · 2026Article
- What is in a name? Rethinking SMUG1 in genome maintenance.NAR cancer · 2025Review
- SMUG1 DNA glycosylase modulates reward behaviour through regulation of olfactory receptor gene expression.Nucleic acids research · 2025Article
- Article
- Unprocessed genomic uracil as a source of DNA replication stress in cancer cells.Molecular cell · 2024Article
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- DNA Glycosylases Define the Outcome of Endogenous Base Modifications.International journal of molecular sciences · 2023Review
- UV-DDB as a General Sensor of DNA Damage in Chromatin: Multifaceted Approaches to Assess Its Direct Role in Base Excision Repair.International journal of molecular sciences · 2023Review
- UV-DDB stimulates the activity of SMUG1 during base excision repair of 5-hydroxymethyl-2'-deoxyuridine moieties.Nucleic acids research · 2023Article
- The Curcumin Analog PAC Is a Potential Solution for the Treatment of Triple-Negative Breast Cancer by Modulating the Gene Expression of DNA Repair Pathways.International journal of molecular sciences · 2023Article
- Ionic strength modulates excision of uracil by SMUG1 from nucleosome core particles.DNA repair · 2023Article
- Urinary Measurement of Epigenetic DNA Modifications and 8-oxodG as Possible Noninvasive Markers of Colon Cancer Evolution.International journal of molecular sciences · 2022Article
- A regulatory network comprising let-7 miRNA and SMUG1 is associated with good prognosis in ER+ breast tumours.Nucleic acids research · 2022Article
- FANCD2 maintains replication fork stability during misincorporation of the DNA demethylation products 5-hydroxymethyl-2'-deoxycytidine and 5-hydroxymethyl-2'-deoxyuridine.Cell death & disease · 2022Article
- The pH-Dependence of the Hydration of 5-Formylcytosine: an Experimental and Theoretical Study.Chembiochem : a European journal of chemical biology · 2022Article
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- Insertion/deletion and microsatellite alteration profiles in induced pluripotent stem cells.Stem cell reports · 2021Article
- Review
- The Multiple Cellular Roles of SMUG1 in Genome Maintenance and Cancer.International journal of molecular sciences · 2021Review
- Retracted Article: Divergent synthesis of 5-substituted pyrimidine 2'-deoxynucleosides and their incorporation into oligodeoxynucleotides for the survey of uracil DNA glycosylases.Chemical science · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Deamination of cytosine (C), 5-methylcytosine (mC) and 5-hydroxymethylcytosine (hmC) occurs spontaneously in mammalian DNA with several hundred deaminations occurring in each cell every day. The resulting potentially mutagenic mispairs of uracil (U), thymine (T) or 5-hydroxymethyluracil (hmU) with guanine (G) are substrates for repair by various DNA glycosylases. Here, we show that targeted inactivation of the mouse Smug1 DNA glycosylase gene is sufficient to ablate nearly all hmU-DNA excision activity as judged by assay of tissue extracts from knockout mice as well as by the resistance of their embryo fibroblasts to 5-hydroxymethyldeoxyuridine toxicity. Inactivation of Smug1 when combined with inactivation of the Ung uracil-DNA glycosylase gene leads to a loss of nearly all detectable uracil excision activity. Thus, SMUG1 is the dominant glycosylase responsible for hmU-excision in mice as well as the major UNG-backup for U-excision. Both Smug1-knockout and Smug1/Ung-double knockout mice breed normally and remain apparently healthy beyond 1 year of age. However, combined deficiency in SMUG1 and UNG exacerbates the cancer predisposition of Msh2(-/-) mice suggesting that when both base excision and mismatch repair pathways are defective, the mutagenic effects of spontaneous cytosine deamination are sufficient to increase cancer incidence but do not preclude mouse development.
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