Efficient surface expression of platelet GPIIb-IIIa requires both subunits.

Density of Platelet GPIIb-IIIa and Bleeding Severity in Iranian Patients with Glanzmann’s Thrombasthenia

Monoclonal antibodies bound to subunits of the integrin GPIIb-IIIa are internalized and interfere with filopodia formation and platelet aggregation.

The monoclonal antibodies Tab and AP3 are directed, respectively, against GPIIb and GPIIIa, the subunits of the platelet fibrinogen receptor. When added together to platelets, these antibodies prevent adenosine diphosphate (ADP)-induced platelet aggregation, despite normal fibrinogen binding (Newman et al, Blood 69:668, 1987). To explore the cellular requirements of aggregation after fibrinogen...

PURIFICATION AND CHARACTERIZATION OF THE HUMAN PLATELET FIBRINOGEN RECEPTOR, GpIIb/IIIa COMPLEX

Platelet GpIIb/IIIa is a member of the integrin family of structurally related adhesion receptors, and adhesive proteins, such as fibrinogen. Ligand binding requires platelet activation by an agonist to convert the receptor to a state where it is capable to bind the ligand. In addition to this a modification, induction of the surface expression and ligand-binding function of an additional pool ...

Direct interaction of iron-regulated surface determinant IsdB of Staphylococcus aureus with the GPIIb/IIIa receptor on platelets.

The interaction of bacteria with platelets is implicated in the pathogenesis of endovascular infections, including infective endocarditis, of which Staphylococcus aureus is the leading cause. Several S. aureus surface proteins mediate aggregation of platelets by fibrinogen- or fibronectin-dependent processes, which also requires specific antibodies. In this study S. aureus was grown in iron-lim...

Lack of influence of the COX inhibitors metamizol and diclofenac on platelet GPIIb/IIIa and P-selectin expression in vitro

BACKGROUND: The effect of non-steroidal anti-inflammatory drugs (NSAIDs) for reduced platelet aggregation and thromboxane A2 synthesis has been well documented. However, the influence on platelet function is not fully explained. Aim of this study was to examine the influence of the COX-1 inhibiting NSAIDs, diclofenac and metamizol on platelet activation and leukocyte-platelet complexes, in vitr...