ArticleNucleic acids research2004
Activation of cryptic 3' splice sites within introns of cellular genes following gene entrapment.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 16 citations in OpenAlex.
- Mutant non-coding RNA resource in mouse embryonic stem cells.Disease models & mechanisms · 2021Article
- Identification of an epithelial cell receptor responsible for Clostridium difficile TcdB-induced cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Role of connexin 43 in Helicobacter pylori VacA-induced cell death.Infection and immunity · 2014Article
- Gene-trap mutagenesis identifies mammalian genes contributing to intoxication by Clostridium perfringens ε-toxin.PloS one · 2011Article
- StARD13(Dlc-2) RhoGap mediates ceramide activation of phosphatidylglycerolphosphate synthase and drug response in Chinese hamster ovary cells.Molecular biology of the cell · 2008Article
- Modeling insertional mutagenesis using gene length and expression in murine embryonic stem cells.PloS one · 2007Article
- Mutagenesis of diploid mammalian genes by gene entrapment.Nucleic acids research · 2006Article
- Hypomorphic mutation in hnRNP U results in post-implantation lethality.Transgenic research · 2005Article
- Post-entrapment genome engineering: first exon size does not affect the expression of fusion transcripts generated by gene entrapment.Genome research · 2005Article
- Discovery of mammalian genes that participate in virus infection.BMC cell biology · 2004Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Gene trap vectors developed for genome-wide mutagenesis can be used to study factors governing the expression of exons inserted throughout the genome. For example, entrapment vectors consisting of a partial 3'-terminal exon [i.e. a neomycin resistance gene (Neo), a poly(A) site, but no 3' splice site] were typically expressed following insertion into introns, from cellular transcripts that spliced to cryptic 3' splice sites present either within the targeting vector or in the adjacent intron. A vector (U3NeoSV1) containing the wild-type Neo sequence preferentially disrupted genes that spliced in-frame to a cryptic 3' splice site in the Neo coding sequence and expressed functional neomycin phosphotransferase fusion proteins. Removal of the cryptic Neo 3' splice site did not reduce the proportion of clones with inserts in introns; rather, the fusion transcripts utilized cryptic 3' splice sites present in the adjacent intron or generated by virus integration. However, gene entrapment with U3NeoSV2 was considerably more random than with U3NeoSV1, consistent with the widespread occurrence of potential 3' splice site sequences in the introns of cellular genes. These results clarify the mechanisms of gene entrapment by U3 gene trap vectors and illustrate features of exon definition required for 3' processing and polyadenylation of cellular transcripts.
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