ArticleBMC molecular biology2007
Reduction of gene repair by selenomethionine with the use of single-stranded oligonucleotides.
Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed, 7 citations in OpenAlex.
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2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe repair of single base mutations in mammalian genes can be directed by single-stranded oligonucleotides in a process known as targeted gene repair. The mechanism of this reaction is currently being elucidated but likely involves a pairing step in which the oligonucleotide align in homologous register with its target sequence and a correction step in which the mutant base is replaced by endogenous repair pathways. This process is regulated by the activity of various factors and proteins that either elevate or depress the frequency at which gene repair takes place.
resultsIn this report, we find that addition of selenomethionine reduces gene repair frequency in a dose-dependent fashion. A correlation between gene repair and altered cell cycle progression is observed. We also find that selenium induces expression of Ref-1 which, in turn, modifies the activity of p53 during the cell cycle.
conclusionWe can conclude from the results that the suppression of gene repair by introduction of selenomethionine occurs through a p53-associated pathway. This result indicates that the successful application of gene repair for treatment of inherited disorders may be hampered by indirect activation of endogenous suppressor functions.
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