Evidence map›Paper›PMID 36574265›Full record

ArticleThe Journal of cell biology2023

TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1.

Jianwen Zhou, Nikoline Lander Rasmussen, Hallvard Lauritz Olsvik, Vyacheslav Akimov, Zehan Hu, Gry Evjen, Stéphanie Kaeser-Pebernard, Devanarayanan Siva Sankar, Carole Roubaty, Pauline Verlhac and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  11. Investigating Protein-Protein Interactions of Autophagy-Involved TNIP1.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Structural basis for TNIP1 binding to FIP200 during mitophagy.The Journal of biological chemistry · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023
    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

17 authors at 4 institutions in 4 countries.

Jianwen Zhou *Department of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0001-6729-1154
Nikoline Lander Rasmussen *Autophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.ORCID 0000-0002-9823-7326
Hallvard Lauritz OlsvikAutophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.ORCID 0000-0003-3489-7461
Vyacheslav AkimovDepartment of Biochemistry and Molecular Biology, Center for Experimental BioInformatics, University of Southern Denmark, Odense, Denmark.
Zehan HuDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Gry EvjenAutophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.ORCID 0000-0002-8313-0593
Stéphanie Kaeser-PebernardDepartment of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0002-6035-6979
Devanarayanan Siva SankarDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Carole RoubatyDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Pauline VerlhacDepartment of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.ORCID 0000-0002-1059-4645
Nicole van de BeekDepartment of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
Fulvio ReggioriDepartment of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.ORCID 0000-0003-2652-2686
Yakubu Princely AbuduAutophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.ORCID 0000-0002-8798-270X
Blagoy BlagoevDepartment of Biochemistry and Molecular Biology, Center for Experimental BioInformatics, University of Southern Denmark, Odense, Denmark.ORCID 0000-0002-3596-0066
Trond LamarkAutophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.ORCID 0000-0001-6338-3342
Terje JohansenAutophagy Research Group, Department of Medical Biology, University of Tromsø-The Arctic University of Norway, Tromsø, Norway.ORCID 0000-0003-1451-9578
Jörn DengjelDepartment of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0002-9453-4614
UiT The Arctic University of Norway · NOUniversity of Fribourg · CHUniversity Medical Center Groningen · NLUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Limitation of excessive inflammation due to selective degradation of pro-inflammatory proteins is one of the cytoprotective functions attributed to autophagy. In the current study, we highlight that selective autophagy also plays a vital role in promoting the establishment of a robust inflammatory response. Under inflammatory conditions, here TLR3-activation by poly(I:C) treatment, the inflammation repressor TNIP1 (TNFAIP3 interacting protein 1) is phosphorylated by Tank-binding kinase 1 (TBK1) activating an LIR motif that leads to the selective autophagy-dependent degradation of TNIP1, supporting the expression of pro-inflammatory genes and proteins. This selective autophagy efficiently reduces TNIP1 protein levels early (0-4 h) upon poly(I:C) treatment to allow efficient initiation of the inflammatory response. At 6 h, TNIP1 levels are restored due to increased transcription avoiding sustained inflammation. Thus, similarly as in cancer, autophagy may play a dual role in controlling inflammation depending on the exact state and timing of the inflammatory response.

Indexed as

AutophagyDNA-Binding ProteinsInflammationProtein Serine-Threonine KinasesHeLa CellsHumansPhosphorylationDNA-Binding ProteinsProtein Serine-Threonine KinasesTBK1 protein, humanTNIP1 protein, human

Identifiers

PMID36574265
PMCPMC9797988
OpenAlexW4313251164

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.