Evidence map›Paper›PMID 32433485›Full record

ArticleScientific reports2020

PGAM5-MAVS interaction regulates TBK1/ IRF3 dependent antiviral responses.

Yu-Qiang Yu, Marta Zielinska, Wei Li, Dominic B Bernkopf, Christiane Silke Heilingloh, Markus F Neurath, Christoph Becker

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. The dual role of PGAM5 in inflammation.Experimental & molecular medicine · 2025
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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 3 countries.

Yu-Qiang YuDepartment of Medicine 1, Friedrich-Alexander-University, Erlangen, Germany.
Marta ZielinskaDepartment of Medicine 1, Friedrich-Alexander-University, Erlangen, Germany.
Wei LiCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, China.
Dominic B BernkopfExperimental Medicine II, Nikolaus-Fiebiger-Center, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Christiane Silke HeilinglohDepartment of Immune Modulation, Friedrich-Alexander-University, Erlangen, Germany.
Markus F NeurathDepartment of Medicine 1, Friedrich-Alexander-University, Erlangen, Germany.
Christoph BeckerDepartment of Medicine 1, Friedrich-Alexander-University, Erlangen, Germany. christoph.becker@uk-erlangen.de.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEMedical University of Lodz · PLNortheast Agricultural University · CNUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viral infections trigger host innate immune responses, characterized by the production of type-I interferons (IFN) including IFNβ. IFNβ induces cellular antiviral defense mechanisms and thereby contributes to pathogen clearance. Accumulating evidence suggests that mitochondria constitute a crucial platform for the induction of antiviral immunity. Here we demonstrate that the mitochondrial protein phosphoglycerate mutase family member 5 (PGAM5) is important for the antiviral cellular response. Following challenge of HeLa cells with the dsRNA-analog poly(I:C), PGAM5 oligomers and high levels of PGAM5 were found in mitochondrial aggregates. Using immunoprecipitation, a direct interaction of PGAM5 with the mitochondrial antiviral-signaling protein (MAVS) was demonstrated. In addition, PGAM5 deficient cells showed diminished expression of IFNβ and IFNβ target genes as compared to WT cells. Moreover, PGAM5 deficient mouse embryonic fibroblasts (MEFs) exhibited decreased phosphorylation levels of IRF3 and TBK1 when challenged with poly(I:C) intracellularly. Finally, PGAM5 deficient MEFs, upon infection with vesicular stomatitis virus (VSV), revealed diminished IFNβ expression and increased VSV replication. Collectively, our study highlights PGAM5 as an important regulator for IFNβ production mediated via the TBK1/IRF3 signaling pathway in response to viral infection.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCells, CulturedFibroblastsHeLa CellsHumansInterferon-betaInterferon Regulatory Factor-3MiceMitochondrial ProteinsPhosphoprotein PhosphatasesPoly I-CProtein Serine-Threonine KinasesRhabdoviridae InfectionsSignal TransductionVesicular stomatitis Indiana virusAdaptor Proteins, Signal TransducingInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanMAVS protein, humanMitochondrial ProteinsPGAM5 protein, humanPhosphoprotein PhosphatasesPoly I-CProtein Serine-Threonine KinasesTBK1 protein, human

Identifiers

PMID32433485
PMCPMC7239892
OpenAlexW3027074586

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.