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Volume 27 Issue 3, March 2009

Artist's impression of a U1 adaptor oligonucleotide (orange) recruiting the U1 snRNP (snRNa in purple) to the 3' end of a target pre-mRNA (blue). Goraczniak et al. show that the resulting inhibition of transcript polyadenylation silences expression of the target gene (p 257). Credit: Ken Eward © Biografx, with data provided by Holger Stark.

Editorial

  • Contrary to Genentech's claims, turning over all in vitro diagnostics to the US Food and Drug Administration (FDA) is the wrong approach to achieve better clinical validation of tests.

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  • One of the most pioneering protein engineers of his generation is also a serial entrepreneur with a flair for spotting new business opportunities.

    • Crispin Littlehales
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  • The Obama administration looks to be a welcome shot in the arm for the scientific endeavor, but the current economic crisis is likely to keep several issues of key interest to biotech firmly on the back burner.

    • Jeffrey L Fox
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Primer

  • Only a subset of genetic variants can be examined in genome-wide surveys for genetic risk factors. How can a fixed set of markers account for the entire genome by acting as proxies for neighboring associations?

    • Eran Halperin
    • Dietrich A Stephan

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Article

  • Goraczniak et al. introduce a gene-silencing method that uses 'U1 adaptors' to block polyadenylation of pre-mRNA in the nucleus. Silencing is stronger when U1 adaptors are combined with siRNAs than when either is used alone.

    • Rafal Goraczniak
    • Mark A Behlke
    • Samuel I Gunderson
    Article
  • Keng et al. characterize the mouse hepatocellular carcinoma genome by using tissue-specific recombinase expression to restrict mobilization of the Sleeping Beauty transposon to the liver. High throughput sequencing of >100,000 insertions sites in mouse tumor nodules identifies potential therapeutic targets.

    • Vincent W Keng
    • Augusto Villanueva
    • David A Largaespada
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