Evidence map›Paper›PMID 23671710›Full record

ArticlePloS one2013

LGP2 plays a critical role in sensitizing mda-5 to activation by double-stranded RNA.

Kay S Childs, Richard E Randall, Stephen Goodbourn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. IFIH1 (MDA5) is required for innate immune detection of intron-containing RNA expressed from the HIV-1 provirus.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Review
  6. Article
  7. Understanding the impact ofFrontiers in molecular biosciences · 2024
    Review
  8. Article
  9. Article
  10. Cellular origins of dsRNA, their recognition and consequences.Nature reviews. Molecular cell biology · 2022
    Review
  11. Article
  12. Article
  13. Host-Viral Interactions in the Pathogenesis of Ulcerative Colitis.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Spatiotemporal dynamics of innate immune signaling via RIG-I-like receptors.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

3 authors at 2 institutions in 1 country.

Kay S ChildsDivision of Biomedical Sciences, St. George's, University of London, London, United Kingdom.
Richard E Randall
Stephen Goodbourn
St George's, University of London · GBUniversity of St Andrews · GB

Funding

Wellcome TrustWellcome Trust 087751/A/08/ZWellcome Trust AL087751/B
6 · The paper itself

Abstract

The DExD/H box RNA helicases retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation associated gene-5 (mda-5) sense viral RNA in the cytoplasm of infected cells and activate signal transduction pathways that trigger the production of type I interferons (IFNs). Laboratory of genetics and physiology 2 (LGP2) is thought to influence IFN production by regulating the activity of RIG-I and mda-5, although its mechanism of action is not known and its function is controversial. Here we show that expression of LGP2 potentiates IFN induction by polyinosinic-polycytidylic acid [poly(I:C)], commonly used as a synthetic mimic of viral dsRNA, and that this is particularly significant at limited levels of the inducer. The observed enhancement is mediated through co-operation with mda-5, which depends upon LGP2 for maximal activation in response to poly(I:C). This co-operation is dependent upon dsRNA binding by LGP2, and the presence of helicase domain IV, both of which are required for LGP2 to interact with mda-5. In contrast, although RIG-I can also be activated by poly(I:C), LGP2 does not have the ability to enhance IFN induction by RIG-I, and instead acts as an inhibitor of RIG-I-dependent poly(I:C) signaling. Thus the level of LGP2 expression is a critical factor in determining the cellular sensitivity to induction by dsRNA, and this may be important for rapid activation of the IFN response at early times post-infection when the levels of inducer are low.

Indexed as

Binding SitesDEAD Box Protein 58DEAD-box RNA HelicasesHEK293 CellsHumansImmunoblottingInterferon-Induced Helicase, IFIH1Interferon Type IPoly I-CProtein BindingReceptors, ImmunologicRNA, Double-StrandedRNA HelicasesRNA InterferenceTranscriptional ActivationTwo-Hybrid System TechniquesDEAD Box Protein 58DEAD-box RNA HelicasesDHX58 protein, humanIFIH1 protein, humanInterferon-Induced Helicase, IFIH1Interferon Type IPoly I-CReceptors, ImmunologicRIGI protein, humanRNA, Double-StrandedRNA HelicasesViral ProteinsV protein, Paramyxovirus

Identifiers

PMID23671710
PMCPMC3650065
OpenAlexW2138553385

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.