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dc.contributor.authorMatsumoto, Saki
dc.contributor.authorCaliskan, Neva
dc.contributor.authorRodnina, Marina V
dc.contributor.authorMurata, Asako
dc.contributor.authorNakatani, Kazuhiko
dc.date.accessioned2018-09-06T14:03:30Z
dc.date.available2018-09-06T14:03:30Z
dc.date.issued2018-08-02
dc.identifier.issn1362-4962
dc.identifier.pmid30085309
dc.identifier.doi10.1093/nar/gky689
dc.identifier.urihttp://hdl.handle.net/10033/621471
dc.description.abstractProgrammed -1 ribosomal frameshifting (-1PRF) is a recoding mechanism to make alternative proteins from a single mRNA transcript. -1PRF is stimulated by cis-acting signals in mRNA, a seven-nucleotide slippery sequence and a downstream secondary structure element, which is often a pseudoknot. In this study we engineered the frameshifting pseudoknot from the mouse mammary tumor virus to respond to a rationally designed small molecule naphthyridine carbamate tetramer (NCTn). We demonstrate that NCTn can stabilize the pseudoknot structure in mRNA and activate -1PRF both in vitro and in human cells. The results illustrate how NCTn-inducible -1PRF may serve as an important component of the synthetic biology toolbox for the precise control of gene expression using small synthetic molecules.en_US
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/us/*
dc.titleSmall synthetic molecule-stabilized RNA pseudoknot as an activator for -1 ribosomal frameshifting.en_US
dc.typeArticleen_US
dc.contributor.departmentHIRI, Helmoltz-Institut für RNA-basierteInfektionsforschung, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany.en_US
refterms.dateFOA2018-09-06T14:03:30Z
dc.source.journaltitleNucleic acids research


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