CD54 / ICAM-1 Antibody - Without BSA and Azide
Mouse Monoclonal Antibody [Clone W-CAM-1; same as Wehi-CAM-1 or 1H4 ]
|Application ||IHC, IF, FC|
|Other Accession||3383, 643447|
|Isotype||Mouse / IgG2b, kappa|
|Clone Names||W-CAM-1; same as Wehi-CAM-1 or 1H4|
|Other Names||Intercellular adhesion molecule 1, ICAM-1, Major group rhinovirus receptor, CD54, ICAM1|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||CD54 / ICAM-1 Antibody - Without BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||ICAM proteins are ligands for the leukocyte adhesion protein LFA-1 (integrin alpha-L/beta-2). During leukocyte trans- endothelial migration, ICAM1 engagement promotes the assembly of endothelial apical cups through ARHGEF26/SGEF and RHOG activation. In case of rhinovirus infection acts as a cellular receptor for the virus.|
|Cellular Location||Membrane; Single-pass type I membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
Recognizes an 85-115kDa protein (variation with cell type), identified as intercellular adhesion molecule (ICAM-1) (Workshop IV). It has 7 potential N-linked glycosylation sites. ICAM-1 is a single chain glycoprotein of Ig supergene family, present on unstimulated endothelial cells (EC) and on a variety of other cell types including activated fibroblasts, EC, macrophages, and lymphocytes. ICAM-1 mediates cell adhesion by binding to integrins CD11a/CD18 (leukocyte adhesion molecule, LFA-1) and to CD11b/CD18 (Mac-1). This interaction enhances antigen-specific T-cell activation. ICAM-1 also binds to CD43 and to Plasmodium falciparum infected RBCs. W-CAM-1 MAb blocks aggregation of cell lines mediated by the ICAM-1 and blocks homotypic binding of purified populations of activated T- and B-lymphocytes and also aggregation of mixed T- and B-cell blasts. It inhibits T-cell adhesion to normal human endothelial cells. Activation induced by cell-cell contact (mixed lymphocyte reaction, T-cell mediated B-cell activation) is significantly inhibited. This MAb blocks elements of both effector arms of immune system (cytotoxic cell function and Ig production).
Boyd AW et. al. Blood, 1989, 73(7):1896-903. | Boyd AW et. al. Proceedings of the National Academy of Sciences, 1988, 85(9):3095 | Wawryk et al. J Clin Pathol 44, 497-501 (1991). | Fecondo et al., Proc. Nat. Acad. Sci. 88(7), 28792882, (1991)
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