Evidence map›Paper›PMID 21914072›Full record

ArticleJournal of viral hepatitis2011

Identification of the IFITM3 gene as an inhibitor of hepatitis C viral translation in a stable STAT1 cell line.

L Yao, H Dong, H Zhu, D Nelson, C Liu, L Lambiase, X Li

Abstract read
In one paragraph

Article in Journal of viral hepatitis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Antiviral Protection by IFITM3 In Vivo.Current clinical microbiology reports · 2018
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. 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

7 authors at 4 institutions in 2 countries.

L YaoDivision of Gastroenterology, Department of Medicine, College of Medicine-Jacksonville, University of Florida, Jacksonville, FL, USA.
H Dong
H Zhu
D Nelson
C Liu
L Lambiase
X Li
University of Florida · USHunan University · CNJacksonville University · USUniversity of Tennessee at Chattanooga · US

Funding

UF CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR029890 · NCRR · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2009 to 2011
$14.4M
Mechanisms of Innate and Adaptive Immunity In HCVR01AI061158 · NIAID · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2005 to 2009
$1.5M
A Multidisciplinary and Translational Approach to Hepatobiliary MalignancyK24CA139570 · NCI · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2010 to 2014
$887k
NCI NIH HHS K24 CA139570NCI NIH HHS K24CA139570-0NCRR NIH HHS UL1 RR029890NCRR NIH HHS UL1RR029890-0NIAID NIH HHS R01 AI061158
6 · The paper itself

Abstract

To investigate the functions of signal transducers and activators of transcription 1 (STAT1)-induced anti-hepatitis C viral (HCV) effects, a stable Huh7.5 cell line (Huh7.5-STAT1ER) was established that constitutively expresses a fusion protein (STAT1ER) of STAT1 and the mouse oestrogen receptor (ER), which forms STAT1ER homodimers after 4-hydroxytamoxifen (4-HT) treatment. This inducible and cytokine/receptor-independent STAT1 activation system allowed us to investigate the anti-HCV effects of STAT1ER activation after inducing IFN-stimulated gene (ISG) expression. The anti-HCV effects of dimerized STAT1ER fusion protein were determined by real-time PCR in a time-dependent fashion post-HCV (JFH-1) infection. HCV (JFH-1) RNA decreased 48% at 72 h after 4-HT treatment. To distinguish the inhibitory effects of STAT1ER activation on HCV RNA replication or HCV internal ribosomal entry site (IRES)-mediated translation, a dicistronic pRL-HL construct was used in the studies. Both cellular (Cap-dependent) and HCV IRES-mediated (Cap-independent) translation were decreased by 63% and 57% at 72 h post-STAT1ER activation in the STAT1ER cell line. In our previous studies, interferon-induced transmembrane protein 3 [(IFITM3) (1-8U)] was found to inhibit HCV RNA replication. Subsequently, elevated expression of the 1-8U gene was confirmed by Western blotting in the Huh7.5-STAT1ER cell line. To further investigate the 1-8U function with both in vivo and in vitro studies, the 1-8U gene was found to suppress cellular and HCV IRES-mediated translation.

Indexed as

Protein BiosynthesisAnimalsCarrier ProteinsCell LineGene ExpressionHepacivirusHumansMembrane ProteinsMiceProtein MultimerizationReal-Time Polymerase Chain ReactionReceptors, EstrogenRecombinant Fusion ProteinsRNA-Binding ProteinsRNA, ViralSTAT1 Transcription FactorafimoxifeneCarrier ProteinsestrophilinIFITM3 protein, humanMembrane ProteinsReceptors, EstrogenRecombinant Fusion ProteinsRNA-Binding ProteinsRNA, ViralSTAT1 Transcription FactorTamoxifenViral Proteins

Identifiers

PMID21914072
PMCPMC3736357
OpenAlexW1545388729

What OpenQuestion holds

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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.