Evidence map›Paper›PMID 28009256›Full record

ArticleeLife2016

Translation initiation by the hepatitis C virus IRES requires eIF1A and ribosomal complex remodeling.

Zane A Jaafar, Akihiro Oguro, Yoshikazu Nakamura, Jeffrey S Kieft

Abstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed.

  1. Article
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  4. UGA4 and YBR062C Regulate Oxidative Stress Tolerance Under Heavy Metal Toxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  18. A highly efficient human cell-free translation system.bioRxiv : the preprint server for biology · 2023
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Zane A JaafarDepartment of Biochemistry and Molecular Genetics, University of Colorado Denver School of Medicine, Aurora, United States.
Akihiro OguroInstitute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoshikazu NakamuraInstitute of Medical Science, The University of Tokyo, Tokyo, Japan.
Jeffrey S KieftDepartment of Biochemistry and Molecular Genetics, University of Colorado Denver School of Medicine, Aurora, United States.ORCID 0000-0002-3718-1891

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Structure, function, and dynamics of viral RNAs and RNA-containing complexesR35GM118070 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI Jeffrey S Kieft · 2016 to 2026
$10.6M
Structural basis of protein synthesis by the hepatitis C virus IRES RNAR01GM081346 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI KIEFT, JEFFREY S · 2008 to 2016
$2.0M
Understanding pathogenic noncoding RNA production in Zika Virus infectionR21AI129569 · NIAID · UNIVERSITY OF COLORADO DENVER · PI KIEFT, JEFFREY S · 2017 to 2018
$419k
Howard Hughes Medical InstituteNCI NIH HHS P30 CA046934NIAID NIH HHS R21 AI129569NIGMS NIH HHS R01 GM081346NIGMS NIH HHS R35 GM118070
6 · The paper itself

Abstract

Internal ribosome entry sites (IRESs) are important RNA-based translation initiation signals, critical for infection by many pathogenic viruses. The hepatitis C virus (HCV) IRES is the prototype for the type 3 IRESs and is also invaluable for exploring principles of eukaryotic translation initiation, in general. Current mechanistic models for the type 3 IRESs are useful but they also present paradoxes, including how they can function both with and without eukaryotic initiation factor (eIF) 2. We discovered that eIF1A is necessary for efficient activity where it stabilizes tRNA binding and inspects the codon-anticodon interaction, especially important in the IRES' eIF2-independent mode. These data support a model in which the IRES binds preassembled translation preinitiation complexes and remodels them to generate eukaryotic initiation complexes with bacterial-like features. This model explains previous data, reconciles eIF2-dependent and -independent pathways, and illustrates how RNA structure-based control can respond to changing cellular conditions.

Indexed as

Host-Pathogen InteractionsInternal Ribosome Entry SitesPeptide Chain Initiation, TranslationalCell LineEukaryotic Initiation Factor-1HepacivirusHumansModels, BiologicalRibosomesViral ProteinsEukaryotic Initiation Factor-1eukaryotic peptide initiation factor-1AInternal Ribosome Entry SitesViral Proteinsbiochemistryeukaryotic initation factor 1A (eIF1A)eukaryotic initation factor 2 (eIF2)Hepatitis C virus (HCV)infectious diseaseinternal ribosome entry site (IRES)microbiologytranslation initiationvirus

Identifiers

PMID28009256
PMCPMC5238962

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.