Fig. 5: Golgi-trapped CDC42 variants induce STING accumulation in the Golgi in a COPI-dependent manner. | Nature Communications

Fig. 5: Golgi-trapped CDC42 variants induce STING accumulation in the Golgi in a COPI-dependent manner.

From: Autoinflammatory patients with Golgi-trapped CDC42 exhibit intracellular trafficking defects leading to STING hyperactivation and ER stress

Fig. 5

A Left: Subcellular stainings of STING, Golgi and nuclei in control and patients’ fibroblasts. Scale bars: 10 µm. Right: Quantification of the degree of STING—Golgi co-localization in each condition. B Measurement of STING—Golgi co-localization in THP-1 cells expressing different forms of CDC42. Quantifications of the degrees of STING—Golgi (C) or CDC42—Golgi (D) co-localizations in THP-1 cells expressing different mutants of CDC42, including some with the K183S/K184S double mutation which inhibits COPI binding. NT: non transfected. In all the graphs, each dot represents the mean value from about 15 cells from one independent experiment. Results are shown as means +/- SEM from at least three biological replicates and the significance levels were calculated using ordinary one-way ANOVA (*P < 0.0192; **P < 0.0098; ***P < 0.0006; ****P < 0,0001). Source data are provided as a Source Data file.

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