Extended Data Fig. 6: DAPK3 is not involved in STING trafficking from ER to Golgi.
From: The tumor suppressor kinase DAPK3 drives tumor-intrinsic immunity through the STING–IFN-β pathway
a, Confocal fluorescence microscopy of THP1-Blue ISG transduced with indicated shRNA and unstimulated or stimulated with 2′,3′-cGAMP (25 μg/ml) for 3 h. Scale bar, 15 μm. b, (Upper) Co-localization of STING/Calreticulin and (lower) STING/GM130 analyzed using Image J software. Data are pooled from three independent experiments (n > 1,500 cells for unstimulated 32 images and cGAMP-stimulated 73 images). c, (Upper) Confocal fluorescence microscopy of THP1-Blue ISG stably expressing GFP-tagged DAPK3(WT) unstimulated or stimulated with 2′,3′-cGAMP (50 μg/ml) for 3 h. Localization of GFP-DAPK3, STING, and TBK1. (Lower) Co-localization of GFP-DAPK3/TBK1, GFP-DAPK3/STING, and TBK1/STING was analyzed using Image J software. Data are pooled from three independent experiments (n > 1,500 cells for unstimulated and cGAMP-stimulated 70 images). Scale bars, 15 μm. d, Schematic representation of human STING mutants. e, (Upper) Immunoprecipitation and immunoblot of HEK293T transfected with plasmid encoding HA-tagged human STING (WT, 1-379), phospho-deficient mutant (3S-3A), or C-terminal deletion mutant (aa 1-340) unstimulated or stimulated with 2′,3′-cGAMP (5 μg/ml) for 2 h, and (lower) immunoblot of whole cell lysates (WCL). Values represented as mean ± s.d. Data in (a, c, e) are representative of three independent experiments.
