ArticlemBio2025
AUP1 and UBE2G2 complex targets STING signaling and regulates virus-induced innate immunity.
Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- From energy metabolic homeostasis to immune remodeling: the role and therapeutic potential of STING signaling in the tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- STING1 negatively regulates translation and replication of foot-and-mouth disease virus independently of interferon and is antagonized by the viral proteins 3C and 2B.Virologica Sinica · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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
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Registered trials
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