JAM-A Antibody – Mouse Monoclonal

The monoclonal antibody M.Ab.F11 recognizes junctional adhesion molecule-A (JAM-A) also known as the human platelet F11-Receptor (F11R) or JAM-1. 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.

1. Kornecki, E et al; Activation of human platelets by a stimulatory monoclonal antibody. J Biol Chem 1990, 265: 10042 2. Naik, U et al; Mechanisms of platelet activation by a stimulatory antibody: cross-linking of a novel platelet receptor for monoclonal antibody F11 with the Fc gamma RII receptor. Biochem J 1995, 310: 155
3. Wang, F et al; Stimulatory antibody-induced activation and selective translocation of protein kinase C isoenzymes in human platelets. Biochem J 1995, 311: 401
4. Sobocka, M et al; Cloning of the human platelet F11 receptor: a cell adhesion molecule member of the immunoglobulin superfamily involved in platelet aggregation. Blood 2000, 95: 2600
5. Babinska, A et al; Two regions of the human platelet F11-receptor (F11R) are critical for platelet aggregation, potentiation and adhesion. Thromb Haemost 2002, 87: 712
6. Babinska, A et al; The F11 receptor (F11R/JAM-A) in atherothrombosis: overexpression of F11R in atherosclerotic plaques. Thromb Haemost 2007, 97: 272
7. Cavusoglu, E et al; Association of plasma levels of F11 receptor/junctional adhesion molecule-A (F11R/JAM-A) with human atherosclerosis. JACC 2007, 50: 1768
8. Koenen, R et al; Regulated release and functional modulation of junctional adhesion molecule A by disintegrin metalloproteinases. Blood 2009, 113: 4799

Small volumes of anti-JAM-A antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS584196 is an antibody targeting JAM-A. Also known as JAM-A, Human, mAb M.Ab.F11. Host: Mouse.