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- W4313251164 abstract "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." @default.
- W4313251164 created "2023-01-06" @default.
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- W4313251164 date "2022-12-27" @default.
- W4313251164 modified "2023-10-18" @default.
- W4313251164 title "TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1" @default.
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- W4313251164 doi "https://doi.org/10.1083/jcb.202108144" @default.
- W4313251164 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36574265" @default.
- W4313251164 hasPublicationYear "2022" @default.
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