Figure 4.
Figure 4. 6his-chem163S was cleaved in control plasma with contact pathway activation, but not in FXI-depleted plasma. The contact pathway was initiated by the addition of kaolin to control or FXI-depleted, plasma-containing microparticles, Ca++, and GPRP. (A) 6His-chem163S (10 μM) was incubated in control plasma and FXI-depleted plasma with contact pathway activation. Aliquots of reactions were removed every 5 minutes, and the level of 6his-chem163S in each aliquot was determined by 6his-chem163S ELISA. (B) FXIa fluorogenic substrate D-LPR-ANSNH-C3H7•2HCl was incubated in control and FXI-depleted plasma with contact pathway activation. The signal was monitored every 15 seconds, and FXIa concentrations were calculated from the interpolation of a FXIa standard curve. Data from 4 independent experiments were pooled to show mean ± standard error of the mean.

6his-chem163S was cleaved in control plasma with contact pathway activation, but not in FXI-depleted plasma. The contact pathway was initiated by the addition of kaolin to control or FXI-depleted, plasma-containing microparticles, Ca++, and GPRP. (A) 6His-chem163S (10 μM) was incubated in control plasma and FXI-depleted plasma with contact pathway activation. Aliquots of reactions were removed every 5 minutes, and the level of 6his-chem163S in each aliquot was determined by 6his-chem163S ELISA. (B) FXIa fluorogenic substrate D-LPR-ANSNH-C3H7•2HCl was incubated in control and FXI-depleted plasma with contact pathway activation. The signal was monitored every 15 seconds, and FXIa concentrations were calculated from the interpolation of a FXIa standard curve. Data from 4 independent experiments were pooled to show mean ± standard error of the mean.

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