TBK1 recruitment to STING activates both IRF3 and NF-κB that mediate immune defense against tumors and viral infections.

ABSTRACT: The induction of type I interferons through the transcription factor interferon regulatory factor 3 (IRF3) is considered a major outcome of stimulator of interferon genes (STING) activation that drives immune responses against DNA viruses and tumors. However, STING activation can also trigger other downstream pathways such as nuclear factor κB (NF-κB) signaling and autophagy, and the roles of interferon (IFN)-independent functions of STING in infectious diseases or cancer are not well understood. Here, we generated a STING mouse strain with a mutation (S365A) that disrupts IRF3 binding and therefore type I interferon induction but not NF-κB activation or autophagy induction. We also generated STING mice with mutations that disrupt the recruitment of TANK-binding kinase 1 (TBK1), which is i

SUBMITTER: Yum S 

PROVIDER: S-EPMC8040795 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature