TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1.
In: The Journal of cell biology, Jg. 222 (2023-02-06), Heft 2
Online
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Zugriff:
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.
(© 2022 Zhou et al.)
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TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1.
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Autor/in / Beteiligte Person: | Zhou, J ; Rasmussen, NL ; Olsvik, HL ; Akimov, V ; Hu, Z ; Evjen, G ; Kaeser-Pebernard, S ; Sankar, DS ; Roubaty, C ; Verlhac, P ; van de Beek N ; Reggiori, F ; Abudu, YP ; Blagoev, B ; Lamark, T ; Johansen, T ; Dengjel, J |
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Zeitschrift: | The Journal of cell biology, Jg. 222 (2023-02-06), Heft 2 |
Veröffentlichung: | New York : Rockefeller University Press, 2023 |
Medientyp: | academicJournal |
ISSN: | 1540-8140 (electronic) |
DOI: | 10.1083/jcb.202108144 |
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