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. 2022 Jul 8;8(27):eabq0084. doi: 10.1126/sciadv.abq0084

Fig. 6. CSK interacts with SPOP and controls LYN activity and IRF activation.

Fig. 6.

(A) Quantitative MS analysis of proteins copurifying with dimerized MyD88. Numbers reflect protein ratios of CM-treated (dimerized) versus nonstimulated samples. Numbers in brackets indicate number of unique peptides identified. (B) Quantitative MS analysis of proteins copurifying with SPOP. Numbers reflect protein ratios of SPOP versus control protein (GyrB). (C) IP/IB analysis using isotype control antibodies or antibodies against endogenous proteins. (D) IP/IB analysis using control or SPOP-deficient RAW264.7 cells and antibodies against endogenous proteins. (E) IP/IB analysis using control or SPOP-deficient RAW264.7 cells expressing FS-MyD88-GyrB and antibodies against the epitope tag (Strep). (F) IP/IB analysis of macrophages derived from MyD88−/− multipotent progenitor cells that were reconstituted with wt or mutant MyD88 [MyD88-AA (SS136/137AA)]. (G) IB analysis of RAW264.7 cells with deletion of SPOP or CSK. (H) IP/IB analysis of RAW264.7 cells with deletion of SPOP or CSK. (I) Nuclear translocation assay of RAW264.7 cells with deletion of CSK. (J) qPCR analysis of RAW264.7 cells with deletion of CSK. Data represent mean ± SD from three independent experiments. **P < 0.01, ***P < 0.005 are determined by two-way ANOVA with Sidak’s multiple comparison test (J).