Evidence map›Paper›PMID 27538435›Full record

ArticleBMC biology2016

The Golgi apparatus acts as a platform for TBK1 activation after viral RNA sensing.

Marie Pourcelot, Naima Zemirli, Leandro Silva Da Costa, Roxane Loyant, Dominique Garcin, Damien Vitour, Ivana Munitic, Aimé Vazquez, Damien Arnoult

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Review
  3. Optineurin Shapes Basal and LPS-Induced Transcriptomes in BV2 Microglia.International journal of molecular sciences · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. The Golgi Apparatus: A Key Player in Innate Immunity.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
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  14. Article
  15. Article
  16. The role of TBK1 in cancer pathogenesis and anticancer immunity.Journal of experimental & clinical cancer research : CR · 2022
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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

9 authors at 6 institutions in 3 countries.

Marie PourcelotINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Naima ZemirliINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Leandro Silva Da CostaINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Roxane LoyantINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Dominique GarcinDepartment of Microbiology and Molecular Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Damien VitourANSES, INRA, ENVA, UPEC, UMR_1161 Virology, LabEx IBEID, Maisons-Alfort, France.
Ivana MuniticLaboratory of Molecular Immunology, Department of Biotechnology, University of Rijeka, Rijeka, Croatia.
Aimé VazquezINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Damien ArnoultINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France. damien.arnoult@inserm.fr.
La Ligue Contre le Cancer · FRHôpital Paul-Brousse · FRInstitut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement · FRUniversité Paris-Saclay · FRUniversity of Geneva · CHUniversity of Rijeka · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAfter viral infection and the stimulation of some pattern-recognition receptors, TANK-binding kinase I (TBK1) is activated by K63-linked polyubiquitination followed by trans-autophosphorylation. While the activated TBK1 induces type I interferon production by phosphorylating the transcription factor IRF3, the precise molecular mechanisms underlying TBK1 activation remain unclear.

resultsWe report here the localization of the ubiquitinated and phosphorylated active form of TBK1 to the Golgi apparatus after the stimulation of RIG-I-like receptors (RLRs) or Toll-like receptor-3 (TLR3), due to TBK1 K63-linked ubiquitination on lysine residues 30 and 401. The ubiquitin-binding protein optineurin (OPTN) recruits ubiquitinated TBK1 to the Golgi apparatus, leading to the formation of complexes in which TBK1 is activated by trans-autophosphorylation. Indeed, OPTN deficiency in various cell lines and primary cells impairs TBK1 targeting to the Golgi apparatus and its activation following RLR or TLR3 stimulation. Interestingly, the Bluetongue virus NS3 protein binds OPTN at the Golgi apparatus, neutralizing its activity and thereby decreasing TBK1 activation and downstream signaling.

conclusionsOur results highlight an unexpected role of the Golgi apparatus in innate immunity as a key subcellular gateway for TBK1 activation after RNA virus infection.

Indexed as

Immunity, InnateCell Cycle ProteinsDEAD Box Protein 58Golgi ApparatusHEK293 CellsHeLa CellsHumansInterferon Regulatory Factor-3Membrane Transport ProteinsPhosphorylationProtein Serine-Threonine KinasesReceptors, ImmunologicRNA VirusesRNA Virus InfectionsSignal TransductionToll-Like Receptor 3Cell Cycle ProteinsDEAD Box Protein 58Interferon Regulatory Factor-3Membrane Transport ProteinsOPTN protein, humanProtein Serine-Threonine KinasesReceptors, ImmunologicRIGI protein, humanS10 protein, Bluetongue virusTBK1 protein, humanTLR3 protein, humanToll-Like Receptor 3Transcription Factor TFIIIAViral Nonstructural Proteins

Identifiers

PMID27538435
PMCPMC4991008
OpenAlexW2513876189

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.