Fig. 4.
Fig. 4. Binding of the PAC-1 MoAb to CHO cells expressing normal and mutant GPIIb/IIIa receptors. CHO cells were transfected with vector alone (Mock), mutant GPIIb and normal GPIIIa (Patient LW), and normal or wild-type GPIIb and GPIIIa (WT) cDNA constructs. The cells were incubated with FITC–PAC-1 in the presence of the GPIIIa-specific LIBS antibody AP539 or a control anti-GPIIIa-specific antibody AP3.40 Flow cytometric analyses were performed and data are presented as mean fluorescence intensity (MFI) ± standard deviation (SD) from five separate experiments. *A two-tailed Student's t-test was performed showing that the binding of PAC-1 to WT cells in the presence of AP5 was significantly greater than the binding in the presence of AP3 (P < .004), while the binding of PAC-1 to AP5-activated Patient LW (P = .35) transfected cells was not greater than the binding in the presence of AP3.

Binding of the PAC-1 MoAb to CHO cells expressing normal and mutant GPIIb/IIIa receptors. CHO cells were transfected with vector alone (Mock), mutant GPIIb and normal GPIIIa (Patient LW), and normal or wild-type GPIIb and GPIIIa (WT) cDNA constructs. The cells were incubated with FITC–PAC-1 in the presence of the GPIIIa-specific LIBS antibody AP539 or a control anti-GPIIIa-specific antibody AP3.40 Flow cytometric analyses were performed and data are presented as mean fluorescence intensity (MFI) ± standard deviation (SD) from five separate experiments. *A two-tailed Student's t-test was performed showing that the binding of PAC-1 to WT cells in the presence of AP5 was significantly greater than the binding in the presence of AP3 (P < .004), while the binding of PAC-1 to AP5-activated Patient LW (P = .35) transfected cells was not greater than the binding in the presence of AP3.

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