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Article

Lack of the DNA glycosylases MYH and OGG1 in the cancer prone double mutant mouse does not increase mitochondrial DNA mutagenesis.

DNA repair - 1 Mar 2012

Halsne Ruth, Esbensen Ying, Wang Wei, Scheffler Katja, Suganthan Rajikala, Bjørås Magnar, Eide Lars

Abstract excerpt

Reactive oxygen species (ROS) are formed as natural byproducts during aerobic metabolism and readily induce premutagenic base lesions in the DNA. The 8-oxoguanine DNA glycosylase (OGG1) and MutY homolog 1 (MYH) synergistically prevent mutagenesis and cancer formation in mice. Their localization in the mitochondria as well as in the nucleus suggests that mutations in mitochondrial DNA (mtDNA) contribute to the...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 22209780
DOI: 10.1016/j.dnarep.2011.12.001

Genes

OGG1

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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Lack of the DNA glycosylases MYH and OGG1 in the cancer prone double mutant mouse does not increase mitochondrial DNA mutagenesis.PMID 22209780Read ↗

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