ArticleJournal of nucleic acids2010
Mouse WRN Helicase Domain Is Not Required for Spontaneous Homologous Recombination-Mediated DNA Deletion.
Article in Journal of nucleic acids, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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Who cites it
3 citing papers in PubMed.
- Induction of homologous recombination following in utero exposure to DNA-damaging agents.DNA repair · 2013Article
- A conditional mouse model for measuring the frequency of homologous recombination events in vivo in the absence of essential genes.Molecular and cellular biology · 2011Article
- Dissection of a mouse eye for a whole mount of the retinal pigment epithelium.Journal of visualized experiments : JoVE · 2011Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Werner syndrome is a rare disorder that manifests as premature aging and age-related diseases. WRN is the gene mutated in WS, and is one of five human RecQ helicase family members. WS cells exhibit genomic instability and altered proliferation, and in vitro studies suggest that WRN has a role in suppressing homologous recombination. However, more recent studies propose that other RecQ helicases (including WRN) promote early events of homologous recombination. To study the role of WRN helicase on spontaneous homologous recombination, we obtained a mouse with a deleted WRN helicase domain and combined it with the in vivo pink-eyed unstable homologous recombination system. In this paper, we demonstrate that WRN helicase is not necessary for suppressing homologous recombination in vivo contrary to previous reports using a similar mouse model.
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Registered trials
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