Skip to main content
. 2025 Aug 9;18:10777–10793. doi: 10.2147/JIR.S541656

Figure 1.

Figure 1

Molecular mechanism of the cGAS-STING signaling. Double-stranded DNA (dsDNA)—from microbes, damaged tissues or dead cells, and injured mitochondria—present in the cytoplasm will be sensed by cyclic GMP-AMP synthase (cGAS). Then cGAS will catalyze ATP and GTP into the second messenger 2′,3′-cyclic GMP-AMP (cGAMP), which will further activate the stimulator of interferon genes (STING) that located at the endoplasmic reticulum in a conformational change of oligomerization. The activated STING will move to Golgi. At Golgi, STING will recruit and phosphorylate the TANK-binding kinase 1 (TBK1) and/or inhibitor of kappa B kinase (IKK), thereafter phosphorylating interferon regulatory factor 3 (IRF3) into dimerization and inhibitor of nuclear factor-kappa B (IκB) into degradation, resulting in IRF3 and nuclear factor-kappa B (NF-κB) activation and translocation into the nucleus to induce transcription of type I interferon (IFN-I) and interferon-stimulated genes (ISGs) as well as proinflammatory cytokines, such as IL-1β, IL-6, TNF-α.