Figure 4. CXCR1 mutants coupled to Gα₁₅.

(A) Activation of PLCβ₂ by CXCR1 through Gα₁₅ proteins. COS-7 cells were cotransfected with equal amounts of cDNA (0.3 µg per well per component) encoding either pSG5, PLCβ₂, Gα₁₅, CXCR1 wild type (WT), Gα₁₅ plus WT, or PLCβ₂ plus WT. Inositol phosphates were measured 1 hours after treatment in the presence (shaded bars) or absence (open bars) of IL-8 (40 nM). Data are mean ± SEM of replicate wells. ** P<0.01, Gα₁₅+WT (+IL-8) vs. Gα₁₅+WT (−IL-8). (B) CXCR1 mutants coupled to Gα₁₅. Basal and IL-8-stimulated inositol phosphate (IP) accumulation in COS-7 cells transiently co-transfected with WT (0.3 µg) or mutant CXCR1 (0.3 µg) and Gα₁₅ (0.3 µg). Data for mutants are summarized from 3–7 experiments, each performed in triplicate, and are expressed as a percentage of WT CXCR1 baseline determined in parallel. The results are mean ± SEM. ** P<0.01, vs. WT+ Gα₁₅ (in the absence of IL-8).