Evidence map›Paper›PMID 26100021›Full record

ArticleMolecular and cellular biology2015

Fine-Tuning of the RIG-I-Like Receptor/Interferon Regulatory Factor 3-Dependent Antiviral Innate Immune Response by the Glycogen Synthase Kinase 3/β-Catenin Pathway.

Kashif Aziz Khan, Florence Dô, Alexandre Marineau, Priscilla Doyon, Jean-François Clément, James R Woodgett, Bradley W Doble, Marc J Servant

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. MicroRNA Interference in Hepatic Host-Pathogen Interactions.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. MicroRNA Involvement in Signaling Pathways During Viral Infection.Frontiers in cell and developmental biology · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

8 authors at 3 institutions in 1 country.

Kashif Aziz KhanFaculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada.
Florence DôFaculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada.
Alexandre MarineauFaculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada.
Priscilla DoyonFaculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada.
Jean-François ClémentFaculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada.
James R WoodgettLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Bradley W DobleStem Cell and Cancer Research Institute, McMaster University, Hamilton, Ontario, Canada.
Marc J ServantFaculty of Pharmacy, Université de Montréal, Montréal, Québec, Canada marc.servant@umontreal.ca.
Université de Montréal · CAMcMaster University · CAMount Sinai Hospital · CA

Funding

Canadian Institutes of Health Research MOP-74711Canadian Institutes of Health Research MOP-84571
6 · The paper itself

Abstract

Induction of an antiviral innate immune response relies on pattern recognition receptors, including retinoic acid-inducible gene 1-like receptors (RLR), to detect invading pathogens, resulting in the activation of multiple latent transcription factors, including interferon regulatory factor 3 (IRF3). Upon sensing of viral RNA and DNA, IRF3 is phosphorylated and recruits coactivators to induce type I interferons (IFNs) and selected sets of IRF3-regulated IFN-stimulated genes (ISGs) such as those for ISG54 (Ifit2), ISG56 (Ifit1), and viperin (Rsad2). Here, we used wild-type, glycogen synthase kinase 3α knockout (GSK-3α(-/-)), GSK-3β(-/-), and GSK-3α/β double-knockout (DKO) embryonic stem (ES) cells, as well as GSK-3β(-/-) mouse embryonic fibroblast cells in which GSK-3α was knocked down to demonstrate that both isoforms of GSK-3, GSK-3α and GSK-3β, are required for this antiviral immune response. Moreover, the use of two selective small-molecule GSK-3 inhibitors (CHIR99021 and BIO-acetoxime) or ES cells reconstituted with the catalytically inactive versions of GSK-3 isoforms showed that GSK-3 activity is required for optimal induction of antiviral innate immunity. Mechanistically, GSK-3 isoform activation following Sendai virus infection results in phosphorylation of β-catenin at S33/S37/T41, promoting IRF3 DNA binding and activation of IRF3-regulated ISGs. This study identifies the role of a GSK-3/β-catenin axis in antiviral innate immunity.

Indexed as

Animalsbeta CateninCell Line, TumorDEAD Box Protein 58DEAD-box RNA HelicasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHeLa CellsHumansImmunity, InnateInterferon Regulatory Factor-3Interferon Type IMiceMice, KnockoutPhosphorylationbeta CateninDEAD Box Protein 58DEAD-box RNA HelicasesGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseInterferon Regulatory Factor-3Interferon Type IIRF3 protein, humanReceptors, ImmunologicRIGI protein, humanRNA, Small Interfering

Identifiers

PMID26100021
PMCPMC4525315
OpenAlexW2268301683

What OpenQuestion holds

Textmetadata
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.