炎症抑制因子TNIP1/ABIN-1在其LIR的TBK1磷酸化后通过自噬降解。

IF 14.6 1区生物学 Q1 CELL BIOLOGY

Autophagy Pub Date : 2023-10-01 Epub Date: 2023-03-09 DOI:10.1080/15548627.2023.2185013

Nikoline L Rasmussen, Jianwen Zhou, Hallvard Olsvik, Stéphanie Kaeser-Pebernard, Trond Lamark, Joern Dengjel, Terje Johansen

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引用次数: 0

摘要

炎症抑制因子TNIP1/ABIN-1对于控制炎症和细胞死亡途径以避免这些途径的潜在危险的持续激活是重要的。我们现在发现，在通过poly（I:C）处理激活TLR3后的早期（0-4小时），TNIP1通过选择性大自噬/自噬快速降解，以允许促炎基因和蛋白质的表达。几个小时后（6小时），TNIP1水平再次升高，以抵消持续的炎症信号。TBK1介导的TNIP1-LIR基序的磷酸化通过刺激与Atg8家族蛋白的相互作用来调节TNIP1的选择性自噬。这是TNIP1的一种新的调节水平，其蛋白水平对控制炎症信号传导至关重要。

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The inflammation repressor TNIP1/ABIN-1 is degraded by autophagy following TBK1 phosphorylation of its LIR.

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.

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来源期刊

Autophagy 生物-细胞生物学

CiteScore

21.30

自引率

2.30%

发文量

277

审稿时长

1 months

期刊介绍： Autophagy is a peer-reviewed journal that publishes research on autophagic processes, including the lysosome/vacuole dependent degradation of intracellular material. It aims to be the premier journal in the field and covers various connections between autophagy and human health and disease, such as cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease. Autophagy is interested in all experimental systems, from yeast to human. Suggestions for specialized topics are welcome. The journal accepts the following types of articles: Original research, Reviews, Technical papers, Brief Reports, Addenda, Letters to the Editor, Commentaries and Views, and Articles on science and art. Autophagy is abstracted/indexed in Adis International Ltd (Reactions Weekly), EBSCOhost (Biological Abstracts), Elsevier BV (EMBASE and Scopus), PubMed, Biological Abstracts, Science Citation Index Expanded, Web of Science, and MEDLINE.