dc.contributor.author | Rasmussen, Nikoline Lander | |
dc.contributor.author | Zhou, Jianwen | |
dc.contributor.author | Olsvik, Hallvard Lauritz | |
dc.contributor.author | Kaeser-Pebernard, Stéphanie | |
dc.contributor.author | Lamark, Trond | |
dc.contributor.author | Dengjel, Joern | |
dc.contributor.author | Johansen, Terje | |
dc.date.accessioned | 2024-03-25T09:32:36Z | |
dc.date.available | 2024-03-25T09:32:36Z | |
dc.date.issued | 2023-03-09 | |
dc.description.abstract | The 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.citation | Rasmussen, Zhou, Olsvik, Kaeser-Pebernard, Lamark, Dengjel, Johansen. The inflammation repressor TNIP1/ABIN-1 is degraded by autophagy following TBK1 phosphorylation of its LIR. Autophagy. 2023 | en_US |
dc.identifier.cristinID | FRIDAID 2139037 | |
dc.identifier.doi | 10.1080/15548627.2023.2185013 | |
dc.identifier.issn | 1554-8627 | |
dc.identifier.issn | 1554-8635 | |
dc.identifier.uri | https://hdl.handle.net/10037/33254 | |
dc.language.iso | eng | en_US |
dc.publisher | Taylor & Francis | en_US |
dc.relation.journal | Autophagy | |
dc.relation.projectID | Kreftforeningen: 190214 | en_US |
dc.relation.projectID | Norges forskningsråd: 249884 | en_US |
dc.rights.accessRights | openAccess | en_US |
dc.rights.holder | Copyright 2023 The Author(s) | en_US |
dc.title | The inflammation repressor TNIP1/ABIN-1 is degraded by autophagy following TBK1 phosphorylation of its LIR | en_US |
dc.type.version | acceptedVersion | en_US |
dc.type | Journal article | en_US |
dc.type | Tidsskriftartikkel | en_US |
dc.type | Peer reviewed | en_US |