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dc.contributor.authorRasmussen, Nikoline Lander
dc.contributor.authorZhou, Jianwen
dc.contributor.authorOlsvik, Hallvard Lauritz
dc.contributor.authorKaeser-Pebernard, Stéphanie
dc.contributor.authorLamark, Trond
dc.contributor.authorDengjel, Joern
dc.contributor.authorJohansen, Terje
dc.date.accessioned2024-03-25T09:32:36Z
dc.date.available2024-03-25T09:32:36Z
dc.date.issued2023-03-09
dc.description.abstractThe inflammatory repressor TNIP1/ABIN-1 is important for keeping in check inflammatory and cell-death pathways to avoid potentially dangerous sustained activation of these pathways. We have now found that TNIP1 is rapidly degraded by selective macroautophagy/autophagy early (0–4 h) after activation of TLR3 by poly(I:C)-treatment to allow expression of pro-inflammatory genes and proteins. A few hours later (6 h), TNIP1 levels rise again to counteract sustained inflammatory signaling. TBK1-mediated phosphorylation of a TNIP1 LIR motif regulates selective autophagy of TNIP1 by stimulating interaction with Atg8-family proteins. This is a novel level of regulation of TNIP1, whose protein level is crucial for controlling inflammatory signaling.en_US
dc.identifier.citationRasmussen, Zhou, Olsvik, Kaeser-Pebernard, Lamark, Dengjel, Johansen. The inflammation repressor TNIP1/ABIN-1 is degraded by autophagy following TBK1 phosphorylation of its LIR. Autophagy. 2023en_US
dc.identifier.cristinIDFRIDAID 2139037
dc.identifier.doi10.1080/15548627.2023.2185013
dc.identifier.issn1554-8627
dc.identifier.issn1554-8635
dc.identifier.urihttps://hdl.handle.net/10037/33254
dc.language.isoengen_US
dc.publisherTaylor & Francisen_US
dc.relation.journalAutophagy
dc.relation.projectIDKreftforeningen: 190214en_US
dc.relation.projectIDNorges forskningsråd: 249884en_US
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2023 The Author(s)en_US
dc.titleThe inflammation repressor TNIP1/ABIN-1 is degraded by autophagy following TBK1 phosphorylation of its LIRen_US
dc.type.versionacceptedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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