Evidence map›Paper›PMID 27106056›Full record

ArticleNucleic acids research2016

Staufen1 promotes HCV replication by inhibiting protein kinase R and transporting viral RNA to the site of translation and replication in the cells.

Updesh Dixit, Ashutosh K Pandey, Priya Mishra, Amitabha Sengupta, Virendra N Pandey

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  4. Liver diseases: epidemiology, causes, trends and predictions.Signal transduction and targeted therapy · 2025
    Review
  5. Emerging roles of stress granules in liver diseases: a comprehensive review.Frontiers in cell and developmental biology · 2025
    Review
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  16. Review
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  19. Article
  20. Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019
    Review
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

5 authors at 1 institution in 1 country.

Updesh DixitDepartment of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers, Rutgers, the State University of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA.
Ashutosh K PandeyDepartment of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers, Rutgers, the State University of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA.
Priya MishraDepartment of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers, Rutgers, the State University of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA.
Amitabha SenguptaDepartment of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers, Rutgers, the State University of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA.
Virendra N PandeyDepartment of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers, Rutgers, the State University of New Jersey, 185 South Orange Avenue, Newark, NJ 07103, USA vnp22@njms.rutgers.edu.
Rutgers, The State University of New Jersey · US

Funding

Proteomics of HCV Replication ComplexR21AI073703 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI PANDEY, VIRENDRA NATH · 2009 to 2010
$429k
FUSE Binding Protein As a Cellular Effector of HCV ReplicationR21DK083560 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI PANDEY, VIRENDRA NATH · 2010 to 2011
$427k
NIAID NIH HHS R21 AI073703NIDDK NIH HHS R21 DK083560
6 · The paper itself

Abstract

Persistent hepatitis C virus (HCV) infection leads to chronic hepatitis C (CHC), which often progresses to liver cirrhosis (LC) and hepatocellular carcinoma (HCC). The molecular mechanisms that establish CHC and cause its subsequent development into LC and HCC are poorly understood. We have identified a cytoplasmic double-stranded RNA binding protein, Stau1, which is crucial for HCV replication. In this study, Stau1 specifically interacted with the variable-stem-loop region in the 3' NTR and domain IIId of the HCV-IRES in the 5' NTR, and promoted HCV replication and translation. Stau1 coimmunoprecipitates HCV NS5B and a cell factor, protein kinase R (PKR), which is critical for interferon-induced cellular antiviral and antiproliferative responses. Like Stau1, PKR displayed binding specificity to domain IIId of HCV-IRES. Stau1 binds to PKR and strongly inhibits PKR-autophosphorylation. We demonstrated that the transport of HCV RNA on the polysomes is Stau1-dependent, being mainly localized in the monosome fractions when Stau1 is downregulated and exclusively localized in the polysomes when Stau1 is overexpressed. Our findings suggest that HCV may appropriate Stau1 to its advantage to prevent PKR-mediated inhibition of eIF2α, which is required for the synthesis of HCV proteins for translocation of viral RNA genome to the polysomes for efficient translation and replication.

Indexed as

Protein BiosynthesisVirus ReplicationBinding SitesCell LineCytoskeletal ProteinseIF-2 KinaseGenome, ViralHepacivirusHepatitis CHumansPhosphorylationPolyribosomesProtein BindingProtein TransportRNA-Binding ProteinsRNA-Dependent RNA PolymeraseCytoskeletal ProteinseIF-2 KinaseNS-5 protein, hepatitis C virusRNA-Binding ProteinsRNA-Dependent RNA PolymeraseRNA, ViralSTAU1 protein, humanUntranslated RegionsViral Nonstructural Proteins

Identifiers

PMID27106056
PMCPMC4914112
OpenAlexW2338117252

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.