GO curators for mouse genes have assigned the following annotations to the gene product of Ogg1. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes the enzyme responsible for the excision of 8-oxoguanine, a mutagenic base byproduct which occurs as a result of exposure to reactive oxygen. The action of this enzyme includes lyase activity for chain cleavage. Alternative splicing of the C-terminal region of this gene classifies splice variants into two major groups, type 1 and type 2, depending on the last exon of the sequence. Type 1 alternative splice variants end with exon 7 and type 2 end with exon 8. All variants share the N-terminal region in common, which contains a mitochondrial targeting signal that is essential for mitochondrial localization. Many alternative splice variants for this gene have been described, but the full-length nature for every variant has not been determined. [provided by RefSeq, Aug 2008]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Ogg1
participates in the following biological processes:
Arai T et al. (2003) Cell proliferation in liver of Mmh/Ogg1-deficient mice enhances mutation frequency because of the presence of 8-hydroxyguanine in DNA. Cancer Res, 63:4287-92. (PubMed:12874039)
Conlon KA et al. (2005) The murine DNA glycosylase NEIL2 (mNEIL2) and human DNA polymerase beta bind microtubules in situ and in vitro. DNA Repair (Amst), 4:419-31. (PubMed:15725623)
de Souza-Pinto NC et al. (2001) Repair of 8-oxodeoxyguanosine lesions in mitochondrial dna depends on the oxoguanine dna glycosylase (OGG1) gene and 8-oxoguanine accumulates in the mitochondrial dna of OGG1-defective mice. Cancer Res, 61:5378-81. (PubMed:11454679)
Freedman SD et al. (1999) A membrane lipid imbalance plays a role in the phenotypic expression of cystic fibrosis in cftr(-/-) mice. Proc Natl Acad Sci U S A, 96:13995-4000. (PubMed:10570187)
Klungland A et al. (1999) Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damage. Proc Natl Acad Sci U S A, 96:13300-5. (PubMed:10557315)
Mootha VK et al. (2003) Integrated analysis of protein composition, tissue diversity, and gene regulation in mouse mitochondria. Cell, 115:629-40. (PubMed:14651853)
Osterod M et al. (2002) A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA base damage. Oncogene, 21:8232-9. (PubMed:12447686)
Osterod M et al. (2001) Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice. Carcinogenesis, 22:1459-63. (PubMed:11532868)
Pagliarini DJ et al. (2008) A mitochondrial protein compendium elucidates complex I disease biology. Cell, 134:112-23. (PubMed:18614015)
Rosenquist TA et al. (1997) Cloning and characterization of a mammalian 8-oxoguanine DNA glycosylase. Proc Natl Acad Sci U S A, 94:7429-34. (PubMed:9207108)
Trapp C et al. (2007) Deficiency of the Cockayne syndrome B (CSB) gene aggravates the genomic instability caused by endogenous oxidative DNA base damage in mice. Oncogene, 26:4044-8. (PubMed:17213818)