AUP1 and UBE2G2 complex targets STING signaling and regulates virus-induced innate immunity.

ABSTRACT: Stimulator of interferon genes (STING) is an endoplasmic reticulum (ER) signaling adaptor that is essential for the host immune response triggered by DNA pathogens. Precise regulation of STING is crucial for maintaining a balanced immune response and preventing harmful autoinflammation. Activation of STING requires its translocation from the ER to the Golgi apparatus. However, the mechanisms that maintain STING in its resting state remain largely unclear. Here, we find that deficiency of the ancient ubiquitous protein 1 (AUP1) causes spontaneous activation of STING and enhances the expression of type I interferons (IFNs) under resting conditions. Furthermore, deficiency of UBE2G2, a cofactor of AUP1, also promotes the abnormal activation of STING. AUP1 deficiency significantl

SUBMITTER: Wang X-T 

PROVIDER: S-EPMC12077101 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature