Clathrin-associated AP-1 controls termination of STING signalling.

ABSTRACT: Stimulator of interferon genes (STING) functions downstream of cyclic GMP-AMP synthase in DNA sensing or as a direct receptor for bacterial cyclic dinucleotides and small molecules to activate immunity during infection, cancer and immunotherapy^1-10. Precise regulation of STING is essential to ensure balanced immune responses and prevent detrimental autoinflammation^11-16. After activation, STING, a transmembrane protein, traffics from the endoplasmic reticulum to the Golgi, where its phosphorylation by the protein kinase TBK1 enables signal transduction^17-20. The mechanism that ends STING signalling at the Golgi remains unknown. Here we show that adaptor protein complex 1 (AP-1) controls the termination of STING-dependent immune activation. We find that AP-1

SUBMITTER: Liu Y 

PROVIDER: S-EPMC9605868 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature