Figure 6.
Figure 6. Binding of anti-GPIbα mAbs to transfected CHO cells. (A) Schematic representation of GPIbα showing the deletion mutation and epitopes of anti-GPIbα mAbs. (B-C) The binding of AK2, VM16d, and WM23 to CHO cells expressing WT (▪) is indistinguishable from that of the Mut GPIbα (□; n = 3, P > .05). Data are represented by the mean channel fluorescence. The mAb binding is specific because the binding to CHO β/IX cells (▦; cells lacking GPIbα) is negligible. The binding of AK2 and VM16d was compared with that of WM23, whose epitope is outside the VWF-binding domain.

Binding of anti-GPIbα mAbs to transfected CHO cells. (A) Schematic representation of GPIbα showing the deletion mutation and epitopes of anti-GPIbα mAbs. (B-C) The binding of AK2, VM16d, and WM23 to CHO cells expressing WT (▪) is indistinguishable from that of the Mut GPIbα (□; n = 3, P > .05). Data are represented by the mean channel fluorescence. The mAb binding is specific because the binding to CHO β/IX cells (▦; cells lacking GPIbα) is negligible. The binding of AK2 and VM16d was compared with that of WM23, whose epitope is outside the VWF-binding domain.

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