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Hepatitis-C-virus-like internal ribosome entry sites displace eIF3 to gain access to the 40S subunit

Author

Listed:
  • Yaser Hashem

    (Howard Hughes Medical Institute (HHMI), Columbia University
    Columbia University)

  • Amedee des Georges

    (Howard Hughes Medical Institute (HHMI), Columbia University
    Columbia University)

  • Vidya Dhote

    (SUNY Downstate Medical Center)

  • Robert Langlois

    (Columbia University)

  • Hstau Y. Liao

    (Columbia University)

  • Robert A. Grassucci

    (Columbia University
    Columbia University)

  • Tatyana V. Pestova

    (SUNY Downstate Medical Center)

  • Christopher U. T. Hellen

    (SUNY Downstate Medical Center)

  • Joachim Frank

    (Howard Hughes Medical Institute (HHMI), Columbia University
    Columbia University
    Columbia University)

Abstract

A sub-nanometre reconstruction of a 40S complex containing eIF3 and a hepatitis C virus (HCV)-like internal ribosome entry site (IRES) shows that the IRES displaces eIF3 from the 40S and sequesters it to gain access to the 40S subunit.

Suggested Citation

  • Yaser Hashem & Amedee des Georges & Vidya Dhote & Robert Langlois & Hstau Y. Liao & Robert A. Grassucci & Tatyana V. Pestova & Christopher U. T. Hellen & Joachim Frank, 2013. "Hepatitis-C-virus-like internal ribosome entry sites displace eIF3 to gain access to the 40S subunit," Nature, Nature, vol. 503(7477), pages 539-543, November.
    • Handle: RePEc:nat:nature:v:503:y:2013:i:7477:d:10.1038_nature12658
    DOI: 10.1038/nature12658
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    Cited by:

    1. Yang Cao & Huachun Liu & Shannon S. Lu & Krysten A. Jones & Anitha P. Govind & Okunola Jeyifous & Christine Q. Simmons & Negar Tabatabaei & William N. Green & Jimmy. L. Holder & Soroush Tahmasebi & Al, 2023. "RNA-based translation activators for targeted gene upregulation," Nature Communications, Nature, vol. 14(1), pages 1-12, December.

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