Journal article
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TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1
DOKPE
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Zhou, Jianwen
ORCID
University of Fribourg
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Rasmussen, Nikoline Lander
ORCID
University of Tromsø
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Olsvik, Hallvard Lauritz
ORCID
University of Tromsø
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Akimov, Vyacheslav
University of Southern Denmark
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Hu, Zehan
University of Fribourg
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Evjen, Gry
ORCID
University of Tromsø
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Kaeser-Pebernard, Stéphanie
ORCID
University of Fribourg
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Sankar, Devanarayanan Siva
University of Fribourg
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Roubaty, Carole
University of Fribourg
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Verlhac, Pauline
ORCID
University of Groningen
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van de Beck, Nicole
University of Groningen
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Reggiori, Fulvio
ORCID
University of Groningen
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Abudu, Yakubu Princely
ORCID
University of Tromsø
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Blagoev, Blagoy
ORCID
University of Southern Denmark
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Lamark, Trond
ORCID
University of Tromsø
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Johansen, Terje
ORCID
University of Tromsø
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Dengjel, Jörn
ORCID
University of Fribourg
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Published in:
- Journal of Cell Biology. - Rockefeller University Press. - 2022, vol. 222, no. 2
English
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 TBK1 (Tank-binding kinase 1) activating a LIR motif that leads to the selective autophagy-dependent degradation of TNIP1, supporting 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.
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Faculty
- Faculté des sciences et de médecine
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Department
- Département de Biologie
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Language
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Classification
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Biology, life sciences
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License
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CC BY-NC-SA
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Open access status
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green
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Identifiers
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Persistent URL
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https://folia.unifr.ch/unifr/documents/323024
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