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Gene Review

Ogg1  -  8-oxoguanine DNA-glycosylase 1

Mus musculus

Synonyms: Mmh, N-glycosylase/DNA lyase
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Disease relevance of Ogg1

  • Here, we demonstrate that deficiencies in Myh and Ogg1 predispose 65.7% of mice to tumors, predominantly lung and ovarian tumors, and lymphomas [1].
  • We found that lung adenoma/carcinoma spontaneously developed in Ogg1 knockout mice approximately 1.5 years after birth in which 8-oxoG was found to accumulate in their genomes [2].
  • The rate of developing malignant tumors in Ogg1 knockout mice was also significantly higher (88.5%; squamous cell carcinomas, 73.1%; sarcomas, 15.4%) than in wild-type mice (50.0%; squamous cell carcinomas, 41.7%; sarcomas, 8.3%) [3].
  • Results: Inflammatory lesions induced in the gastric mucosa of H. pylori-infected mice, corresponding to a moderate gastritis, were less severe in Ogg1(-/-) than in Wt Big Blue mice [4].
  • During the course of study the mice appeared normal, although a decrease of body weight gain in both Ogg1(-/-) and Ogg1(+/+) mice exposed to KBrO3, and some kidney malfunction in KBrO3 treated Ogg1(-/-) mice was observed [5].

High impact information on Ogg1

  • Csb(-/-) mice crossed with a strain defective in base excision repair (Ogg1) demonstrated no enhanced neurodegenerative phenotype [6].
  • Mmh/Ogg1 gene inactivation results in accumulation of 8-hydroxyguanine in mice [7].
  • Expression of the mouse Ogg1 protein in the homozygous ogg1(-/-) cell line restored the ability to remove 8-OxoG in the NTS [8].
  • To assess the role of the Ogg1 DNA glycosylase in the transcription-coupled repair (TCR) of the mutagenic lesion, 7, 8-dihydro-8oxoguanine (8-OxoG), we have investigated the removal of this lesion in wild-type and ogg1(-/-) null mouse embryo fibroblast (MEF) cell lines [8].
  • Ogg1 mRNA is expressed in several mouse tissues; highest levels were detected in testes [9].

Biological context of Ogg1

  • However, no remarkable up-regulation of Ogg1-an oxidative DNA damage repair gene-was observed in the tumor areas, but the expression of Trail-an apoptosis-signaling ligand gene-was significantly down-regulated in the tumor tissues [10].
  • Combined, these observations suggest that a cooperative function between Ogg1 and Mutyh exists to prevent 8-oxoG-related mutagenesis in mammals [11].
  • Cell proliferation in liver of Mmh/Ogg1-deficient mice enhances mutation frequency because of the presence of 8-hydroxyguanine in DNA [12].
  • We have analysed the steady-state levels and repair kinetics of oxidative DNA modifications in cells of homozygous ogg1(-/-) null mice, which are deficient in Ogg1 protein, a DNA repair glycosylase that removes the miscoding base 8-hydroxyguanine (8-oxoG) from the genome [13].
  • The Ogg1 gene is localized to the mouse chromosome 6E [14].

Anatomical context of Ogg1

  • Furthermore, Ogg1 was not up-regulated in murine B cells from germinal centers [15].
  • The expression and activity of 8-oxoguanosine DNA-glycosylase (Ogg1), a key enzyme responsible forthe clearance of the oxidized DNA base 8-hydroxy-2'-deoxyguanosine (oxo8dG), was determined in the cerebellum (CB) and the caudate and the putamen (CP) of male Balb/c, ICR, and C57BL/J mice [16].
  • In these conditions, the H. pylori-SS1 infection in the Ogg1(-/-) mice did not induce a mutagenic effect at the gastric epithelial cells level, either after 3 or 6 months [4].
  • 8-Oxodeoxyguanosine glycosylase (Ogg1) mRNA was up-regulated in response to bromate treatment in kidney but not thyroid [17].
  • Surprisingly, when Ogg1(-/-) and Ogg1(+/+) mice were sacrificed at 52 weeks, no tumor formation could be found in kidney or other organs such as lung, liver, spleen, thymus, stomach and intestine [5].

Associations of Ogg1 with chemical compounds

  • Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases [18].
  • 8-Oxoguanine formation induced by chronic UVB exposure makes Ogg1 knockout mice susceptible to skin carcinogenesis [3].
  • Oxidative purine modifications including 8-oxoG were quantified by means of an alkaline elution assay in combination with Fpg protein, the bacterial functional analogue of Ogg1 protein [13].
  • The mouse Ogg1 protein acts efficiently on duplexes in which the 8-OH-Gua is paired with a cytosine but is inactive on 8-OH-Gua: Ade pair, consistently with its proposed biological role in the avoidance of mutations [14].
  • The Mth1 mRNA level decreased soon after kainate administration and then quickly recovered beyond the basal level, and a continuously increased MTH1 protein level was observed, whereas the Ogg1 mRNA level remained constant [19].

Other interactions of Ogg1

  • Functional cooperation of Ogg1 and Mutyh in preventing G: C-->T: a transversions in mice [11].
  • Ogg1 knockout-associated lung tumorigenesis and its suppression by Mth1 gene disruption [2].

Analytical, diagnostic and therapeutic context of Ogg1

  • Partial hepatectomy was performed on Ogg1(+/-) and Ogg1(-/-) mice after being treated with KBrO(3) for 12 weeks [12].
  • Western blot analysis and repair activity in extracts from Ogg1(-/-) mice revealed that OGG1 was responsible for the efficient 8-oxoG removal from prenatal mice [20].
  • We studied oxidative damage to DNA in broncho-alveolar lavage cells, lungs, and liver after 4 x 1.5 h inhalations of DEP (20 mg/m3) in Ogg1-/- and wild type (WT) mice with similar extent of inflammation [21].


  1. Deficiencies in mouse Myh and Ogg1 result in tumor predisposition and G to T mutations in codon 12 of the K-ras oncogene in lung tumors. Xie, Y., Yang, H., Cunanan, C., Okamoto, K., Shibata, D., Pan, J., Barnes, D.E., Lindahl, T., McIlhatton, M., Fishel, R., Miller, J.H. Cancer Res. (2004) [Pubmed]
  2. Ogg1 knockout-associated lung tumorigenesis and its suppression by Mth1 gene disruption. Sakumi, K., Tominaga, Y., Furuichi, M., Xu, P., Tsuzuki, T., Sekiguchi, M., Nakabeppu, Y. Cancer Res. (2003) [Pubmed]
  3. 8-Oxoguanine formation induced by chronic UVB exposure makes Ogg1 knockout mice susceptible to skin carcinogenesis. Kunisada, M., Sakumi, K., Tominaga, Y., Budiyanto, A., Ueda, M., Ichihashi, M., Nakabeppu, Y., Nishigori, C. Cancer Res. (2005) [Pubmed]
  4. Deficiency in OGG1 Protects against Inflammation and Mutagenic Effects Associated with H. pylori Infection in Mouse. Touati, E., Michel, V., Thiberge, J.M., Avé, P., Huerre, M., Bourgade, F., Klungland, A., Labigne, A. Helicobacter (2006) [Pubmed]
  5. The study using wild-type and Ogg1 knockout mice exposed to potassium bromate shows no tumor induction despite an extensive accumulation of 8-hydroxyguanine in kidney DNA. Arai, T., Kelly, V.P., Minowa, O., Noda, T., Nishimura, S. Toxicology (2006) [Pubmed]
  6. Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome mice. Laposa, R.R., Huang, E.J., Cleaver, J.E. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  7. Mmh/Ogg1 gene inactivation results in accumulation of 8-hydroxyguanine in mice. Minowa, O., Arai, T., Hirano, M., Monden, Y., Nakai, S., Fukuda, M., Itoh, M., Takano, H., Hippou, Y., Aburatani, H., Masumura, K., Nohmi, T., Nishimura, S., Noda, T. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  8. Transcription coupled repair of 8-oxoguanine in murine cells: the ogg1 protein is required for repair in nontranscribed sequences but not in transcribed sequences. Le Page, F., Klungland, A., Barnes, D.E., Sarasin, A., Boiteux, S. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  9. Cloning and characterization of a mammalian 8-oxoguanine DNA glycosylase. Rosenquist, T.A., Zharkov, D.O., Grollman, A.P. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  10. Gene expression analysis on the dicyclanil-induced hepatocellular tumors in mice. Moto, M., Okamura, M., Muguruma, M., Ito, T., Jin, M., Kashida, Y., Mitsumori, K. Toxicologic pathology (2006) [Pubmed]
  11. Functional cooperation of Ogg1 and Mutyh in preventing G: C-->T: a transversions in mice. Isogawa, A. Fukuoka Igaku Zasshi (2004) [Pubmed]
  12. Cell proliferation in liver of Mmh/Ogg1-deficient mice enhances mutation frequency because of the presence of 8-hydroxyguanine in DNA. Arai, T., Kelly, V.P., Komoro, K., Minowa, O., Noda, T., Nishimura, S. Cancer Res. (2003) [Pubmed]
  13. Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice. Osterod, M., Hollenbach, S., Hengstler, J.G., Barnes, D.E., Lindahl, T., Epe, B. Carcinogenesis (2001) [Pubmed]
  14. Excision repair of 8-hydroxyguanine in mammalian cells: the mouse Ogg1 protein as a model. Boiteux, S., Dhérin, C., Reille, F., Apiou, F., Dutrillaux, B., Radicella, J.P. Free Radic. Res. (1998) [Pubmed]
  15. Normal somatic hypermutation of Ig genes in the absence of 8-hydroxyguanine-DNA glycosylase. Winter, D.B., Phung, Q.H., Zeng, X., Seeberg, E., Barnes, D.E., Lindahl, T., Gearhart, P.J. J. Immunol. (2003) [Pubmed]
  16. Strain-specific differences in the expression and activity of Ogg1 in the CNS. Mosquera, D.I., Stedeford, T., Cardozo-Pelaez, F., Sanchez-Ramos, J. Gene Expr. (2003) [Pubmed]
  17. Molecular biomarkers of oxidative stress associated with bromate carcinogenicity. Delker, D., Hatch, G., Allen, J., Crissman, B., George, M., Geter, D., Kilburn, S., Moore, T., Nelson, G., Roop, B., Slade, R., Swank, A., Ward, W., DeAngelo, A. Toxicology (2006) [Pubmed]
  18. Accumulation of the oxidative base lesion 8-hydroxyguanine in DNA of tumor-prone mice defective in both the Myh and Ogg1 DNA glycosylases. Russo, M.T., De Luca, G., Degan, P., Parlanti, E., Dogliotti, E., Barnes, D.E., Lindahl, T., Yang, H., Miller, J.H., Bignami, M. Cancer Res. (2004) [Pubmed]
  19. MTH1, an oxidized purine nucleoside triphosphatase, suppresses the accumulation of oxidative damage of nucleic acids in the hippocampal microglia during kainate-induced excitotoxicity. Kajitani, K., Yamaguchi, H., Dan, Y., Furuichi, M., Kang, D., Nakabeppu, Y. J. Neurosci. (2006) [Pubmed]
  20. Repair and mutagenesis at oxidized DNA lesions in the developing brain of wild-type and Ogg1-/- mice. Larsen, E., Reite, K., Nesse, G., Gran, C., Seeberg, E., Klungland, A. Oncogene (2006) [Pubmed]
  21. Repeated inhalations of diesel exhaust particles and oxidatively damaged DNA in young oxoguanine DNA glycosylase (OGG1) deficient mice. Risom, L., Dybdahl, M., Møller, P., Wallin, H., Haug, T., Vogel, U., Klungland, A., Loft, S. Free Radic. Res. (2007) [Pubmed]
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