Flow cytometry: Use at a 1:10 dilution. Immunoprecipitation Functional application: Antibody directly stimulates the aggregation and granule secretion of human platelets. Western blotting: Use at a 1:10 dilution The optimal dilution for a specific application should be determined by the researcher.
Restrictions
For Research Use only
Format
Liquid
Buffer
1 mL of 100 µg/mL 0.2 µm filtered antibody solution in PBS containing 0.1% protein stabilizer.
Junctional adhesion molecule-1 (JAM-1) is a cell adhesion molecule (CAM). JAM-1 is a member of the immunoglobulin superfamily found on the surface of human platelets and at intercellular junctions of endothelial cells and epithelial cells. JAM-1 belongs together with JAM-2 and JAM-3 to a family of adhesion proteins with a V-C2 immunoglobulin domain organization. JAM plays an important role in tight junctions where it is involved in cell-to-cell adhesion through homophilic interaction. It co-distributes with other tight junction components such as ZO-1, 7H6 antigen, cingulin and occludin. In humans JAM-1 plays a role in platelet aggregation, secretion, adhesion and spreading. JAM-1 is a membrane protein involved in 2 distinct processes initiated on the platelet surface. Antibody-induced platelet aggregation and secretion both depend on FcgammaRII and GPIIb/IIIa intergrin, a process that may be involved in pathophysiological processes associated with certain thrombocytopenias. Antibody mediated platelet adhesion independent from FcgammaRII or fibrinogen receptor and that appears to place a role in physiological processes associated with platelet adhesion and aggregation. A physiological role for the JAM-1 protein was demonstrated by its phosphorylation after the stimulation of platelets by thrombin and collagen. A pathophysiological role for the JAM-1 antibodies in patients with thrombocytopenia. Adhesion of platelets through the F11R resulted in events characteristic of the action of cell adhesion molecules (CAMs). Recent data suggests a role for JAM-1 in the adhesion of platelets to cytokine-inflamed endothelial cells and thus in thrombosis and atherosclerosis induces in non-denuded blood vessels by inflammatory processes.