Figure 5
Figure 5. Hypothetical model for the role of GPIbα in the mechanism of action of rFVIIa. (A) On the resting platelet, the interaction between rFVIIa and the GPIb-IX-V complex (depicted as “Ib”) does not occur, as the resting platelet does not express negatively charged phospholipids, and presumably because the GPIb-IX-V complex is not in a rFVIIa-binding membrane environment. (B) After activation of the platelet, rFVIIa is able to interact with the GPIb-IX-V complex. This interaction is critically dependent on the negatively charged surface but may also involve translocation of the GPIb-IX-V complex to an anionic or lipid raft region of the platelet surface. Alternatively, the interaction might require a conformational change with the GPIb-IX-V complex. The interaction of rFVIIa with GPIb results in acceleration of Xa generation.

Hypothetical model for the role of GPIbα in the mechanism of action of rFVIIa. (A) On the resting platelet, the interaction between rFVIIa and the GPIb-IX-V complex (depicted as “Ib”) does not occur, as the resting platelet does not express negatively charged phospholipids, and presumably because the GPIb-IX-V complex is not in a rFVIIa-binding membrane environment. (B) After activation of the platelet, rFVIIa is able to interact with the GPIb-IX-V complex. This interaction is critically dependent on the negatively charged surface but may also involve translocation of the GPIb-IX-V complex to an anionic or lipid raft region of the platelet surface. Alternatively, the interaction might require a conformational change with the GPIb-IX-V complex. The interaction of rFVIIa with GPIb results in acceleration of Xa generation.

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