ArticleNucleic acids research1998
Up-regulation of base excision repair correlates with enhanced protection against a DNA damaging agent in mouse cell lines.
Article in Nucleic acids research, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Molecular editing ofRSC medicinal chemistry · 2024Article
- Detection of Oxidatively Modified Base Lesion(s) in Defined DNA Sequences by FLARE Quantitative PCR.Methods in molecular biology (Clifton, N.J.) · 2023Article
- The Role of DNA Damage in Neural Plasticity in Physiology and Neurodegeneration.Frontiers in cellular neuroscience · 2022Review
- The prognostic significance of Flap Endonuclease 1 (FEN1) in breast ductal carcinoma in situ.Breast cancer research and treatment · 2021Article
- Eukaryotic Base Excision Repair: New Approaches Shine Light on Mechanism.Annual review of biochemistry · 2019Review
- Potent and specific MTH1 inhibitors targeting gastric cancer.Cell death & disease · 2019Article
- Age-related declines in α-Klotho drive progenitor cell mitochondrial dysfunction and impaired muscle regeneration.Nature communications · 2018Article
- DNA repair after oxidative stress: current challenges.Current opinion in toxicology · 2018Article
- Mitochondrial DNA damage: molecular marker of vulnerable nigral neurons in Parkinson's disease.Neurobiology of disease · 2014Article
- Quantitative PCR-based measurement of nuclear and mitochondrial DNA damage and repair in mammalian cells.Methods in molecular biology (Clifton, N.J.) · 2014Article
- Biological and therapeutic relevance of nonreplicative DNA polymerases to cancer.Antioxidants & redox signaling · 2013Review
- Oxidative Stress and DNA Damage in Human Gastric Carcinoma: 8-Oxo-7'8-dihydro-2'-deoxyguanosine (8-oxo-dG) as a Possible Tumor Marker.International journal of molecular sciences · 2013Article
- Altered expression of base excision repair genes in response to high glucose-induced oxidative stress in HepG2 hepatocytes.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- Analysis of DNA damage and repair in nuclear and mitochondrial DNA of animal cells using quantitative PCR.Methods in molecular biology (Clifton, N.J.) · 2012Article
- The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency.Mechanisms of ageing and development · 2011Review
- Folate deficiency regulates expression of DNA polymerase β in response to oxidative stress.Free radical biology & medicine · 2011Article
- Arsenic biotransformation as a cancer promoting factor by inducing DNA damage and disruption of repair mechanisms.Molecular biology international · 2011Article
- Base excision repair and design of small molecule inhibitors of human DNA polymerase β.Cellular and molecular life sciences : CMLS · 2010Review
- DNA base excision repair activities in mouse models of Alzheimer's disease.Neurobiology of aging · 2009Article
- Mechanisms of stress resistance in Snell dwarf mouse fibroblasts: enhanced antioxidant and DNA base excision repair capacity, but no differences in mitochondrial metabolism.Free radical biology & medicine · 2009Article
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Authors and funding
8 authors.
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Abstract
DNA polymerase beta is required in mammalian cells for the predominant pathway of base excision repair involving single nucleotide gap filling DNA synthesis. Here we examine the relationship between oxidative stress, cellular levels of DNA polymerase beta and base excision repair capacity in vitro , using mouse monocytes and either wild-type mouse fibroblasts or those deleted of the DNA polymerase beta gene. Treatment with an oxidative stress-inducing agent such as hydrogen peroxide, 3-morpholinosydnonimine, xanthine/xanthine oxidase or lipopolysaccharide was found to increase the level of DNA polymerase beta in both monocytes and fibroblasts. Base excision repair capacity in vitro , as measured in crude cell extracts, was also increased by lipopolysaccharide treatment in both cell types. In monocytes lipopolysaccharide-mediated up-regulation of the base excision repair system correlated with increased resistance to the monofunctional DNA alkylating agent methyl methanesulfonate. By making use of a quantitative PCR assay to detect lesions in genomic DNA we show that lipopolysaccharide treatment of fibroblast cells reduces the incidence of spontaneous DNA lesions. This effect may be due to the enhanced DNA polymerase beta-dependent base excision repair capacity of the cells, because a similar decrease in DNA lesions was not observed in cells deficient in base excision repair by virtue of DNA polymerase beta gene deletion. Similarly, fibroblasts treated with lipopolysaccharide were more resistant to methyl methanesulfonate than untreated cells. This effect was not observed in cells deleted of the DNA polymerase beta gene. These results suggest that the DNA polymerase beta-dependent base excision repair pathway can be up-regulated by oxidative stress-inducing agents in mouse cell lines.
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