|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||32583 Da|
|Other Names||Junctional adhesion molecule A, JAM-A, Junctional adhesion molecule 1, JAM-1, Platelet F11 receptor, Platelet adhesion molecule 1, PAM-1, CD321, F11R, JAM1, JCAM|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-terminus of human JAM1 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||JAM1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Seems to play a role in epithelial tight junction formation. Appears early in primordial forms of cell junctions and recruits PARD3 (PubMed:11489913). The association of the PARD6- PARD3 complex may prevent the interaction of PARD3 with JAM1, thereby preventing tight junction assembly (By similarity). Plays a role in regulating monocyte transmigration involved in integrity of epithelial barrier (By similarity). Ligand for integrin alpha- L/beta-2 involved in memory T-cell and neutrophil transmigration (PubMed:11812992). Involved in platelet activation (PubMed:10753840).|
|Cellular Location||Cell junction, tight junction. Cell membrane; Single-pass type I membrane protein. Note=Localized at tight junctions of both epithelial and endothelial cells|
|Tissue Location||Expressed in endothelium, epithelium and leukocytes (at protein level).|
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Provided below are standard protocols that you may find useful for product applications.
Junctional Adhesion Molecules (JAMs) are components and regulators of the well-characterized epithelial and endothelial tight junction. JAM is selectively concentrated at intercellular junctions of endothelial and epithelial cells of different origins. Microscopy shows that JAM codistributes with tight junction components at the apical region of the intercellular cleft. A mAb directed to JAM (BV11) was found to inhibit spontaneous and chemokine-induced monocyte transmigration through an endothelial cell monolayer in vitro. Systemic treatment of mice with BV11 mAb blocked monocyte infiltration upon chemokine administration in subcutaneous air pouches (1). The human protein shares a highly conserved structure and sequence with the murine protein. However it is distinct in that it is constitutively expressed on circulating neutrophils, monocytes, platelets and lymphocyte subsets (2).
1. Martin-Padura I, et al. J Cell Biol 142(1):117-27, 1998
2. Williams LA, et al. Mol Immunol 36(17):1175-88.
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