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Anti-Human Junctional Adhesion Molecule-1(JAM-1), Clone BV16 mAb
 
Catalog No:   HM2098     (datasheet)
Brand:   Hycult Biotechnology
Quantity:   100 µg
Price:   $495.00   add to cart

Category/Sub:   Monoclonal Antibodies / Adhesion Molecule Antibodies
Notes:   The antibody can be used for flow cytometry and immunohistology on frozen sections or cell monolayers.
Isotype:   Mouse IgG1
Description:   Junctional adhesion molecule-1 (JAM-1) also known as the human platelet F11-Receptor (F11R) 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 codistributes with other tight junction components as ZO-1, 7H6 antigen, cingulin and occludin. JAM-1 plays a role in platelet aggregation, secretion, adhesion, spreading. In the platelet F11R/Jam-1 is a membrane protein involved in 2 distinct processes initiated on the platelet surface. 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. Antibody mediated platelet adhesion independent from FcgammaRII or fibrinogen receptor and that appears to play a role in physiological processes associated with platelet adhesion and aggregation. A physiological role for the F11R/Jam-1 protein was demonstrated by its phosphorylation after the stimulation of platelets by thrombin and collagen. A pathophysiological role for the F11R/Jam-1 was revealed by demonstrating the presence of F11R/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 F11R/Jam-1 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.


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