Figure 6
Figure 6. IAC-1 binding to α2β1 on CVX-stimulated platelets in plasma is not observed in the absence of αIIbβ3. (A) Flow cytometric analysis of membrane glycoprotein expression of the Glanzmann platelets. Control platelets in plasma (□) or platelets from a patient with Glanzmann platelets in plasma (⊡) were incubated with AK-7 (anti-α2; 2 μg/mL), AP2 (anti-αIIbβ3; 5 μg/mL), AP3 (anti-β3; 5 μg/mL), or 6B4 (anti-GPIb; 2 μg/mL), followed by a 1:10 dilution of rabbit anti–mouse IgG–FITC. (B) Flow cytometric experiments detecting IAC-1, collagen, PAC-1, and anti–P-selectin binding to resting platelets (−) or CVX-stimulated platelets (+) of control (□) or Glanzmann patient (⊡). Data are expressed as the mean ± SEM of at least 2 independent experiments on control platelets and 1 or 2 experiments on Glanzmann platelets.

IAC-1 binding to α2β1 on CVX-stimulated platelets in plasma is not observed in the absence of αIIbβ3. (A) Flow cytometric analysis of membrane glycoprotein expression of the Glanzmann platelets. Control platelets in plasma (□) or platelets from a patient with Glanzmann platelets in plasma (⊡) were incubated with AK-7 (anti-α2; 2 μg/mL), AP2 (anti-αIIbβ3; 5 μg/mL), AP3 (anti-β3; 5 μg/mL), or 6B4 (anti-GPIb; 2 μg/mL), followed by a 1:10 dilution of rabbit anti–mouse IgG–FITC. (B) Flow cytometric experiments detecting IAC-1, collagen, PAC-1, and anti–P-selectin binding to resting platelets (−) or CVX-stimulated platelets (+) of control (□) or Glanzmann patient (⊡). Data are expressed as the mean ± SEM of at least 2 independent experiments on control platelets and 1 or 2 experiments on Glanzmann platelets.

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