Signal transduction pathways activated by CXCL11 isoforms. Recombinant CXCL11(1-73) (□), synthetic CXCL11(1-73) (■), CXCL11(3-73) (▴), CXCL11(5-73) (♦), and CXCL11(7-73) (○) were tested for their ability to increase the [Ca^{2 +}] _i in CHO-CXCR3 cells (A-B). In panel A, a representative dose-response experiment is shown. The inset in panel B shows the average increase in [Ca^{2 +}] _i induced by CXCL11(3-73), CXCL11(5-73), and CXCL11(7-73) at an enlarged scale. For desensitization experiments (C), 0.1 nM intact CXCL11(1-73) was added as the second stimulus. Results represent the mean (± SEM) of 3 or more independent experiments. Alternatively, serum-starved CHO-CXCR3 cells were treated with different concentrations of CXCL11 isoforms. After 5 minutes, the reaction was stopped and cells were lysed. The level of phosphorylated ERK1/2 (■) or PKB/Akt (□) in the cell lysate was determined with specific ELISAs (D). The mean values and standard errors are derived from 2 to 10 experiments. Statistical analysis was performed using the Mann-Whitney U test. Significant differences in ERK1/2 or PKB/Akt phosphorylation compared with control samples are indicated as *P < .05, **P < .01, and ***P < .001.