Extended Data Fig. 4: The PERK-eIF2α cascade is discrete with TBK1-IRF3 and NF-κB signalling and STING-induced autophagy.

(A) Ectopic expression of STING CTD induced the phosphorylation of endogenous eIF2α in HEK293 cells in a dose-dependent manner. (B) Immunofluorescence imaging revealed that STING CTD was distributed in the cytoplasm and the nucleus, distinct from the full-length STING that associates the ER. Scale bars=20 μm. (C) Treatment of PERK inhibitor unaffected the STING-induced autophagy in DLD1 cells, as indicated by LC3 lipidation. Data in A-C represent three independent experiments. (D-E) PERK inhibition did not substantially regulate STING-induced NF-κB signalling activation, either STING versions from human (D), anemone (E), or Drosophila (E), as evidenced by the reporter assays. In D-E, n = 3 independent experiments (mean ± SEM), and P values were indicated by one-way ANOVA with the Bonferroni correction.