Figure 2.

PTMs in STING pathway. PTMs are going along with the life of STING, from activation to degradation. When CDNs bind to STING, STING is recruited and dimerized with the help of reversible oxidation and disulfide bond. SUMOylation and ubiquitination can help STING with oligomerization, while phosphorylation is related to the activation of STING. Then STING transports from ER to Golgi. Palmitoylation and sGAGs could help STING reside on Golgi, thus continuous activation of STING leads to increasing pro-inflammatory cytokines. On the other hand, inhibition of STING happens along with activation to achieve cellular homeostasis. Sequential oxidation inhibits STING dimerization. Dephosphorylation and deubiquitination of STING decrease the oligomerization of STING. Also, carbonylation caused by ROS and alkylation caused by NO₂-FAs can competitively inhibit palmitoylation and block sequential residence of STING on Golgi, thus immune responses are inhibited. In addition, dephosphorylation, ubiquitination and deSUMOylation could facilitate protein degradation to maintain proteostasis.