JAM-A is a surface glycoprotein duplex (32 and 35 kDa) belongingto the immunoglobulin superfamily found on the surface of human platelets and at intercellular junctions of endothelial cells and epithelial cells. JAM-A belongs together with JAM-C (JAM-2) and JAM-B (VE-JAM or JAM-3) to a family of adhesion proteins with a V-C2 immunoglobulin domain organization. JAM-A plays an important role in tight junctions where it is involved in cell-to-cell adhesion through homophilic interactions. It co-distributes with other tight junction components such as ZO-1, 7H6 antigen, cingulin and occludin. Moreover, JAM-A plays a role in platelet aggregation, secretion, adhesion, spreading. In the platelet, JAM-A is a membrane protein involved in 2 distinct processes initiated on the platelet surface. Namely, antibody-induced platelet aggregation and secretion both dependent on FcgammaRII and GPIIb/IIIa integrin, a process that may be involved in pathophysiological processes associated with certain thrombocytopenias and secondly, antibody mediated platelet adhesion independent from FcgammaRII or fibrinogen receptor that appears to play a role in physiological processes associated with platelet adhesion and aggregation. A physiological role for the JAM-A protein was demonstrated by its phosphorylation after the stimulation of platelets by thrombin and collagen. A pathophysiological role for the JAM-A was revealed by demonstrating the presence of JAM-A antibodies in patients with thrombocytopenia. Adhesion of platelets through JAM-A resulted in events characteristic of the action of cell adhesion molecules. Recent data suggests a role for JAM-A in the adhesion of platelets to cytokine-inflamed endothelial cells and thus in thrombosis and atherosclerosis induced in non-denuded blood vessels by inflammatory processes.Synonyms: F11R, JAM-A, JCAM, Junctional adhesion molecule 1, Junctional adhesion molecule A, PAM1, Platelet F11 receptor, Platelet adhesion molecule 1