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Integrin alpha-IIb, encoded by the ITGA2B gene, forms the α subunit of the αIIbβ3 integrin (also known as glycoprotein IIb/IIIa), a key platelet surface receptor involved in platelet aggregation and thrombus formation. It pairs with the beta 3 subunit to mediate platelet-platelet interactions by binding fibrinogen and other adhesive ligands with RGD motifs, facilitating clot formation at sites of vascular injury. Mutations in ITGA2B disrupt the integrin’s function and cause bleeding disorders such as Glanzmann thrombasthenia, a rare autosomal recessive condition marked by defective platelet aggregation. Drugs targeting αIIbβ3 inhibit its interaction with ligands, thereby reducing pathological thrombosis risk but with attendant bleeding risk. Integrin alpha-IIb serves as a therapeutic and diagnostic target in platelet biology and thrombotic disorders
Antagonists block ligand binding to αIIbβ3 integrin, inhibiting platelet aggregation (e.g., preventing fibrinogen binding to the integrin complex)
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