HNF1A 通过介导 TBK1 的自噬降解来调节先天免疫反应和 MAFLD 之间的串扰。
HNF1A regulates the crosstalk between innate immune responses and MAFLD by mediating autophagic degradation of TBK1.
机构信息
Biotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.
Institute of Vaccine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.
出版信息
Autophagy. 2023 Mar;19(3):1026-1027. doi: 10.1080/15548627.2022.2110728. Epub 2022 Aug 11.
Abstract
The selective macroautophagy/autophagy pathway is an important pathway of protein degradation, regulating signal transduction pathways via selective degradation of certain signaling complexes. TBK1 functions as a key protein in innate immunity or metabolic-associated fatty liver disease (MAFLD); however, the degradation of TBK1 has not been fully investigated. Recently, we have found that HNF1A functions as a novel cargo receptor to bridge TBK1 and MAP1LC3/LC3, hence promoting the degradation of TBK1 and regulating antiviral innate immunity and MAFLD.
摘要
选择性巨自噬/自噬途径是蛋白质降解的重要途径，通过选择性降解某些信号转导复合物来调节信号转导途径。TBK1 作为先天免疫或代谢相关脂肪性肝病（MAFLD）中的关键蛋白发挥作用；然而，TBK1 的降解尚未得到充分研究。最近，我们发现 HNF1A 作为一种新型货物受体，连接 TBK1 和 MAP1LC3/LC3，从而促进 TBK1 的降解，并调节抗病毒先天免疫和 MAFLD。
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本文引用的文献
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Hepatocyte nuclear factor 1A suppresses innate immune response by inducing degradation of TBK1 to inhibit steatohepatitis.肝细胞核因子1A通过诱导TBK1降解抑制先天性免疫反应，从而抑制脂肪性肝炎。
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