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. 2023 Jan;103(1):21–37. doi: 10.1124/molpharm.122.000614

Fig. 4.

Fig. 4.

Assessment of functional impact of RGS10 somatic mutations on GPCR-G protein activation and G protein binding. (A) Structural view of selected mutated tolerant (red) and intolerant (blue) residues in RGS10. (B) Coimmunoprecipitation studies show that mutants K89M bound to Gαo-AlF4- while S64T blocked binding. Average whole traces of BRET signal over time (n = 3) are shown comparing WT and 3DMTR somatic mutations in identified tolerant residue Flag-S64T (C) and intolerant residues Flag-K89M (E). BRET amplitude observed from data presented for Flag-S64T (D) and Flag-K89M comparison (F). Tolerant residue Flag-S64T (C–D) led to change of function while intolerant Flag-K89M (E–F) did not change. Error bars represent mean ± S.D. Statistical analysis was performed using one-way ANOVA with Dunnett’s test (**P < 0.005).