Breakup feared after filamin leaves GPIb.

摘要

On damage to vessel walls, exposed extracellular matrix (ECM) proteins trigger a series of events leading to the formation of a vascular plug. ECM-associated VWF plays a critical role in mediating initial platelet recruitment under flow because of the rapid on-rate of binding between VWF and the platelet receptor GPIb/V/IX. A conformational change in VWF induced by binding to ECM proteins is required for GPIb-VWF interactions, restricting platelet recruitment to sites of vascular injury. Alternatively, high-affinity binding of GPIb to VWF can be induced by exogenous modulators such as the bacterial glycopeptide ristocetin, the snake C-type lec-tin botrocetin, or pathologic levels of high shear as is found in stenosed vessels.