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dc.contributor.authorZhou, Jianwen
dc.contributor.authorRasmussen, Nikoline Lander
dc.contributor.authorOlsvik, Hallvard Lauritz
dc.contributor.authorAkimov, Vyacheslav
dc.contributor.authorHu, Zehan
dc.contributor.authorEvjen, Gry
dc.contributor.authorKaeser-Pebernard, Stéphanie
dc.contributor.authorSankar, Devanarayanan Siva
dc.contributor.authorRoubaty, Carole
dc.contributor.authorVerlhac, Pauline
dc.contributor.authorvan de Beck, Nicole
dc.contributor.authorReggiori, Fulvio
dc.contributor.authorAbudu, Yakubu Princely
dc.contributor.authorBlagoev, Blagoy
dc.contributor.authorLamark, Trond
dc.contributor.authorJohansen, Terje
dc.contributor.authorDengjel, Jörn
dc.date.accessioned2023-03-30T07:56:14Z
dc.date.available2023-03-30T07:56:14Z
dc.date.issued2022-12-27
dc.description.abstractLimitation 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.en_US
dc.identifier.citationZhou, Rasmussen, Olsvik, Akimov, Hu, Evjen, Kaeser-Pebernard, Sankar, Roubaty, Verlhac, van de Beck, Reggiori, Abudu, Blagoev, Lamark, Johansen, Dengjel. TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1. Journal of Cell Biology. 2023;222(2)en_US
dc.identifier.cristinIDFRIDAID 2134769
dc.identifier.doi10.1083/jcb.202108144
dc.identifier.issn0021-9525
dc.identifier.issn1540-8140
dc.identifier.urihttps://hdl.handle.net/10037/28889
dc.language.isoengen_US
dc.publisherRockefeller University Pressen_US
dc.relation.journalJournal of Cell Biology
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2023 The Author(s)en_US
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0en_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)en_US
dc.titleTBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1en_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US


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Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
Med mindre det står noe annet, er denne innførselens lisens beskrevet som Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)