Evidence map›Paper›PMID 27086836›Full record

ArticleFEBS letters2016

The TBK1-binding domain of optineurin promotes type I interferon responses.

Netra Pal Meena, Guozhi Zhu, Paul R Mittelstadt, Maria Letizia Giardino Torchia, Marie Pourcelot, Damien Arnoult, Jonathan D Ashwell, Ivana Munitic

Open access · greenAbstract readLetter
In one paragraph

Article in FEBS letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Optineurin Shapes Basal and LPS-Induced Transcriptomes in BV2 Microglia.International journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Optineurin in ocular herpes infection.Experimental eye research · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Noncoding RNAProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Review
  17. Article
  18. Review
  19. Neuroinflammation in frontotemporal dementia.Nature reviews. Neurology · 2019
    Review
  20. Frontiers in immunology · 2018
    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

8 authors at 4 institutions in 3 countries.

Netra Pal MeenaLaboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Guozhi ZhuLaboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Paul R MittelstadtLaboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Maria Letizia Giardino TorchiaLaboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Marie PourcelotINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Damien ArnoultINSERM, UMR_S 1197, Hôpital Paul Brousse, Villejuif, France.
Jonathan D AshwellLaboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Ivana MuniticLaboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
National Cancer Institute · USNational Institutes of Health · USHôpital Paul-Brousse · FRUniversité Paris-Saclay · FR

Funding

Regulation and Consequences of UbiquitinationZ01BC010779 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ASHWELL, JONATHAN · 2007 to 2008
$1.3M
Intramural NIH HHS Z01 BC010779
6 · The paper itself

Abstract

Pathogen-associated molecular pattern (PAMP) recognition leads to TANK-binding kinase (TBK1) polyubiquitination and activation by transautophosphorylation, resulting in IFN-β production. Here, we describe a mouse model of optineurin insufficiency (OptnΔ(157) ) in which the TBK1-interacting N-terminus of optineurin was deleted. PAMP-stimulated cells from OptnΔ(157) mice had reduced TBK1 activity, no phosphorylation of optineurin Ser(187) , and mounted low IFN-β responses. In contrast to pull-down assays where the presence of N-terminus was sufficient for TBK1 binding, both the N-terminal and the ubiquitin-binding regions of optineurin were needed for PAMP-induced binding. This report establishes optineurin as a positive regulator TBK1 via a bipartite interaction between these molecules.

Indexed as

AnimalsBinding SitesCell Cycle ProteinsEye ProteinsGene Expression RegulationHEK293 CellsHumansInterferon-betaMembrane Transport ProteinsMicePathogen-Associated Molecular Pattern MoleculesPhosphorylationProtein BindingProtein Serine-Threonine KinasesSequence DeletionCell Cycle ProteinsEye ProteinsInterferon-betaMembrane Transport ProteinsOptn protein, mousePathogen-Associated Molecular Pattern MoleculesProtein Serine-Threonine KinasesTbk1 protein, mouseoptineurinTBK1type I interferon

Identifiers

PMID27086836
PMCPMC4879041
OpenAlexW2338707769

What OpenQuestion holds

Textmetadata
LicenceTDM
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.