ArticleJournal of neurochemistry2007
Yeast apurinic/apyrimidinic endonuclease Apn1 protects mammalian neuronal cell line from oxidative stress.
Article in Journal of neurochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Comparative Study of Cytotoxicity, DNA Damage and Oxidative Stress Induced by Heavy Metals Cd(II), Hg(II) and Cr(III) in Yeast.Current microbiology · 2021Article
- Do we age because we have mitochondria?Protoplasma · 2014Review
- The role of base excision repair genes OGG1, APN1 and APN2 in benzo[a]pyrene-7,8-dione induced p53 mutagenesis.Mutation research · 2013Article
- Animal models of mitochondrial DNA transactions in disease and ageing.Experimental gerontology · 2010Review
- The approaches for manipulating mitochondrial proteome.Environmental and molecular mutagenesis · 2010Review
- Contribution of glutathione status to oxidant-induced mitochondrial DNA damage in colonic epithelial cells.Free radical biology & medicine · 2009Article
- Glutathione and apoptosis.Free radical research · 2008Review
- Mitochondrial DNA repair in aging and disease.Mechanisms of ageing and developmentReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) have been implicated as one of the agents responsible for many neurodegenerative diseases. A critical target for ROS is DNA. Most oxidative stress-induced DNA damage in the nucleus and mitochondria is removed by the base excision repair pathway. Apn1 is a yeast enzyme in this pathway which possesses a wider substrate specificity and greater enzyme activity than its mammalian counterpart for removing DNA damage, making it a good therapeutic candidate. For this study we targeted Apn1 to mitochondria in a neuronal cell line derived from the substantia nigra by using a mitochondrial targeting signal (MTS) in an effort to hasten the removal of DNA damage and thereby protect these cells. We found that following oxidative stress, mitochondrial DNA (mtDNA) was repaired more efficiently in cells containing Apn1 with the MTS than controls. There was no difference in nuclear repair. However, cells that expressed Apn1 without the MTS showed enhanced repair of both nuclear and mtDNA. Both Apn1-expressing cells were more resistant to cell death following oxidative stress compared with controls. Therefore, these results reveal that the expression of Apn1 in neurons may be of potential therapeutic benefit for treating patients with specific neurodegenerative diseases.
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Registered trials
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