Fig. 3
From: RASON promotes KRASG12C-driven tumor progression and immune evasion in non-small cell lung cancer
RASON binds to KRASG12C and stabilizes it in the GTP-bound hyperactive state. A, Immunofluorescence staining showing the co-localization of RASON and KRAS in KRASG12C lung cancer cell lines H358 and LLC, as well as in KRASG12C-transformed RAS-less MEF (MEFG12C) cells. Quantification of fluorescence intensity is shown on the right. Scale bar, 10 μm. B, Co-immunoprecipitation assay showing the interaction between RASON and KRASG12C in H23 and MEFG12C cell lines. C, 2D 1H-15N HSQC spectra of 15N-labeled human KRASG12C in the absence and presence of RASON at the indicated molar ratios. D, GST-Raf1-RBD pull-down assay illustrating reduced levels of active GTP-bound KRAS (active RAS) in RASON-KO KRASG12C lung cancer cells. E, NF1-stimulated extrinsic KRASG12C GTPase activity in the presence of RASON measured by GTPase hydrolysis assay (RASON concentrations indicated in the legend). F, Intrinsic KRASG12C GTPase activity in the presence of RASON measured by GTPase hydrolysis assay (RASON concentrations indicated in the legend). Data shown are means ± S.D. and analyzed by two-way ANOVA (E, F). *** p < 0.001; **** p < 0.0001