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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity

Fig. 2

Glycosaminoglycan affinity of C-terminally truncated CXCL10(1–73) is reduced compared to intact CXCL10(1–77). CXCL10(1–77) and CXCL10(1–73) at varying concentrations were sent over the neutravidin-coated CM4 Biosensor chip surface on which biotinylated heparin, HS or CS-A were immobilized. A A schematic illustration of the experimental set-up is shown. Representative SPR sensorgrams are shown (from 4 independent experiments) displaying the affinity for B, C heparin, D-F HS and G-I CS-A of B, E, H CXCL10(1–77), C, F, I CXCL10(1–73) and D, G CXCL4. SPR sensorgrams were obtained after subtracting the baseline signal of the reference channel and a blank of the respective channel. Kinetic parameters were determined from the association phase (1 to 120 s) and dissociation phase (120 to 300 s) of the SPR sensorgrams. The y-axis displays the SPR response in response units (RU). Chemokine accumulation on J heparin, K HS and L CS-A. The maximum signal (Rmax; RU) obtained during injection of CXCL4, CXCL10(1–77) and CXCL10(1–73) was plotted in function of the chemokine concentration. Data were plotted as the mean (± SEM) of 3–4 independent experiments

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