Optimal working dilution should be determined by the investigator.
Restrictions
For Research Use only
Concentration
0.1 mg/mL
Buffer
PBS, 0.02 % sodium azide, 0.1 % bovine serum albumin
Preservative
Sodium azide
Precaution of Use
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C
Storage Comment
Store at 2 - 8 °C.
Target
F11R
(F11 Receptor (F11R))
Alternative Name
CD321 / JAM1
Background
Together with JAM-C (JAM-2) and JAM-B (VE-JAM or JAM-3), JAM-A belongs to a family of adhesion proteins with a V-C2 immunoglobulin domain organization. JAMs are important for a variety of cellular processes, including tight junction assembly, leukocyte transmigration, platelet activation, angiogenesis and virus binding. JAM-A is expressed by endothelial and epithelial cells, platelets, neutrophils, monocytes, lymphocytes and erythrocytes. Like all other JAMs, JAM-A play 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-A also plays an important role in leukocyte transmigration. Leukocyte transmigration can be blocked by antibodies and by soluble JAM-A/Fc fusion proteins. Homophilic JAM-A interactions between leukocytes and the endothelium but also heterophilic interactions of JAM-A with the b2-integrin leukocyte function-associated antigen-1 (LFA-1) are considered to actively guide leukocytes during transmigration. Several studies imply a role of JAM-A in the initiation of atherosclerosis, since JAM-A is upregulated on early atherosclerotic endothelium and adhesion of activated platelets on activated endothelium is mediated by homophilic interactions of JAM-A.Synonyms: F11R, JAM-A, JCAM, Junctional adhesion molecule 1, Junctional adhesion molecule A, PAM1, Platelet F11 receptor, Platelet adhesion molecule 1