E
Edward J. Gunther
Researcher at Yale University
Publications - 8
Citations - 408
Edward J. Gunther is an academic researcher from Yale University. The author has contributed to research in topics: Mutagenesis & DNA. The author has an hindex of 7, co-authored 8 publications receiving 403 citations.
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Targeted mutagenesis of DNA using triple helix-forming oligonucleotides linked to psoralen
TL;DR: The ability to reproducibly and predictably target mutations to sites in intact duplex DNA by using modified oligonucleotides may prove useful as a technique for gene therapy, as an approach to antiviral therapeutics, and as a tool for genetic engineering.
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Site-specific targeting of psoralen photoadducts with a triple helix-forming oligonucleotide: characterization of psoralen monoadduct and crosslink formation
TL;DR: Experiments characterized the photomodification of the targeted region of the supF gene in the context of triple helix formation and a strong strand preference for specific photoadduct formation was detected.
Journal Article
Mutagenesis by 8-methoxypsoralen and 5-methylangelicin photoadducts in mouse fibroblasts: Mutations at cross-linkable sites induced by monoadducts as well as cross-links
TL;DR: Although most of the mutations occurred at potentially cross-linkable sites, these results implicate monoadducts, as well as cross-links, as critical premutagenic lesions in psoralen-treated mammalian cells, and they may aid in the improved design of psoranen-based treatment regimens in the future.
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High efficiency, restriction-deficient in vitro packaging extracts for bacteriophage lambda DNA using a new E.coli lysogen
Journal ArticleDOI
Frequent spontaneous deletions at a shuttle vector locus in transgenic mice
Eric G. Leach,Edward J. Gunther,Toni M. Yeasky,Lisa H. Gibson,Teresa L. Yang-Feng,Peter M. Glazer +5 more
TL;DR: Results suggest that the deletion mutagenesis affecting the transgene sequences in 1139 mice is a locus-specific effect occurring during growth and development, and is proposed that the lambda DNA may have either integrated into an unstable genomic site or created a newly unstable locus in the process of integration.