Evidence map›Paper›PMID 25531441›Full record

ArticlePloS one2014

Deficiency in either 4E-BP1 or 4E-BP2 augments innate antiviral immune responses.

Atef Nehdi, Polen Sean, Izzar Linares, Rodney Colina, Maritza Jaramillo, Tommy Alain

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Emerging translation strategies during virus-host interaction.Wiley interdisciplinary reviews. RNA · 2021
    Review
  9. Infection by the Protozoan ParasiteFrontiers in cellular and infection microbiology · 2020
    Article
  10. Article
  11. Article
  12. 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

6 authors at 5 institutions in 3 countries.

Atef NehdiDepartment of Biochemistry and Goodman Cancer Center, McGill University, Montreal, Quebec H3A 1A3, Canada; College of medicine, King Saud Bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, King Abdulaziz Medical City, National Guard Health Affairs, P.O. Box 22490, Riyadh 11426, Mail Code 1515, Saudi Arabia.
Polen SeanDepartment of Biochemistry and Goodman Cancer Center, McGill University, Montreal, Quebec H3A 1A3, Canada.
Izzar LinaresChildren's Hospital of Eastern Ontario Research Institute, Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada.
Rodney ColinaUniversidad de la República, Laboratorio de Virología Molecular-PDU, Regional Norte Rivera 1350, CP 50000, Salto, Uruguay.
Maritza JaramilloINRS Institut Armand-Frappier Research Centre, 531, boulevard des Prairies, Laval, Quebec, Canada.
Tommy AlainChildren's Hospital of Eastern Ontario Research Institute, Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada.
Wilfrid Laurier University · CAInstitut National de la Recherche Scientifique · CAKing Saud bin Abdulaziz University for Health Sciences · SAMcGill University · CAUniversidad de la República · UY

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Genetic deletion of both 4E-BP1 and 4E-BP2 was found to protect cells against viral infections. Here we demonstrate that the individual loss of either 4E-BP1 or 4E-BP2 in mouse embryonic fibroblasts (MEFs) is sufficient to confer viral resistance. shRNA-mediated silencing of 4E-BP1 or 4E-BP2 renders MEFs resistant to viruses, and compared to wild type cells, MEFs knockout for either 4E-BP1 or 4E-BP2 exhibit enhanced translation of Irf-7 and consequently increased innate immune response to viruses. Accordingly, the replication of vesicular stomatitis virus, encephalomyocarditis virus, influenza virus and Sindbis virus is markedly suppressed in these cells. Importantly, expression of either 4E-BP1 or 4E-BP2 in double knockout or respective single knockout cells diminishes their resistance to viral infection. Our data show that loss of 4E-BP1 or 4E-BP2 potentiates innate antiviral immunity. These results provide further evidence for translational control of innate immunity and support targeting translational effectors as an antiviral strategy.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCell Cycle ProteinsCell LineCytokinesEncephalomyocarditis virusEukaryotic Initiation FactorsFibroblastsHEK293 CellsHumansImmunity, InnateInterferon Regulatory Factor-7MiceOrthomyxoviridaePhosphoproteinsAdaptor Proteins, Signal TransducingCarrier ProteinsCell Cycle ProteinsCytokinesEif4ebp1 protein, mouseEif4ebp2 protein, mouseEukaryotic Initiation FactorsInterferon Regulatory Factor-7Irf7 protein, mousePhosphoproteinsRecombinant ProteinsRNA, Small Interfering

Identifiers

PMID25531441
PMCPMC4273997
OpenAlexW2003154276

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.