Fig. 4.
Fig. 4. Binding of fibrinogen and expression of the ligand-induced conformation depend on disulfide-exchange–induced expression of free thiols and on PDI. / (A) Concentration-dependent effect of pCMPS, bacitracin, and RL90 on binding of FITC-fibrinogen to platelets in autologous plasma stimulated by ADP (diamonds), collagen (squares), thrombin (triangles), and CRP-XL (circles). The total fluorescence at each concentration of the inhibitor was expressed as the percentage of fluorescence in its absence, defined as 100%. Binding in the presence of the inhibitors is shown in solid lines, and binding in the presence of IgG2aascites (a control for the effect of RL90 in ascites) is shown in dotted lines. Data are mean ± SD from 3 different determinations using samples from 3 different donors. (B) Binding of FITC-conjugated PAC-1 under the same conditions as in panel A. (C) Binding of monoclonal PMI-1, followed by FITC-conjugated anti-mouse IgG, under the same conditions as in panel A.

Binding of fibrinogen and expression of the ligand-induced conformation depend on disulfide-exchange–induced expression of free thiols and on PDI.

(A) Concentration-dependent effect of pCMPS, bacitracin, and RL90 on binding of FITC-fibrinogen to platelets in autologous plasma stimulated by ADP (diamonds), collagen (squares), thrombin (triangles), and CRP-XL (circles). The total fluorescence at each concentration of the inhibitor was expressed as the percentage of fluorescence in its absence, defined as 100%. Binding in the presence of the inhibitors is shown in solid lines, and binding in the presence of IgG2aascites (a control for the effect of RL90 in ascites) is shown in dotted lines. Data are mean ± SD from 3 different determinations using samples from 3 different donors. (B) Binding of FITC-conjugated PAC-1 under the same conditions as in panel A. (C) Binding of monoclonal PMI-1, followed by FITC-conjugated anti-mouse IgG, under the same conditions as in panel A.

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