HNF1A regulates the crosstalk between innate immune responses and MAFLD by mediating autophagic degradation of TBK1

Yunfei Qin; Dongbo Qiu; Qi Zhang

doi:10.1080/15548627.2022.2110728

HNF1A regulates the crosstalk between innate immune responses and MAFLD by mediating autophagic degradation of TBK1

Autophagy. 2023 Mar;19(3):1026-1027. doi: 10.1080/15548627.2022.2110728. Epub 2022 Aug 11.

Authors

Yunfei Qin^{1

2}, Dongbo Qiu², Qi Zhang^{1

2}

Affiliations

¹ Biotherapy Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.
² Institute of Vaccine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.

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.

Keywords: Cargo receptor; HNF1A; MAFLD; TBK1; selective autophagy.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Autophagy*
Immunity, Innate
Phosphorylation
Protein Serine-Threonine Kinases* / metabolism
Signal Transduction

Substances

Protein Serine-Threonine Kinases

Grants and funding

This work was supported by the National Natural Science Foundation of China [No. 81970509, 81870449 and 81800559], the Natural Science Foundation of Guangdong Province [2022A1515012223].