|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Solid Phase Sandwich ELISA|
|For the quantitative determination of Human ICAM-1 / CD54 concentration in serum.|
The use of this kit for other sample types need be validated by the end user due to the complexity of natural targets and unpredictable interference.
|The minimum detectable dose of Human ICAM-1 / CD54 is typically less than 7.95 pg/mL. The MDD was determined by adding three standard deviations to the mean optical density value of twenty zero standard replicates and calculating the corresponding concentration.|
|1. 96 well microplate coated with Capture Antibody|
2. Detection Antibody conjugated to HRP
4. Wash Buffer Concentrate
5. Dilution Buffer Concentrate
6. Color Reagent A
7. Color Reagent B
8. Stop Solution
|Unopened Kit: Store at 2 - 8℃|
Opened/Reconstituted Reagents: Please refer to CoA
Intercellular adhesion molecule-1 (ICAM-1, or CD54) is a 90 kDa member of the immunoglobulin (Ig) superfamily and is critical for the firm arrest and transmigration of leukocytes out of blood vessels and into tissues. ICAM-1 is constitutively present on endothelial cells, but its expression is increased by proinflammatory cytokines. The endothelial expression of ICAM-1 is increased in atherosclerotic and transplant-associated atherosclerotic tissue and in animal models of atherosclerosis. Additionally, ICAM-1 has been implicated in the progression of autoimmune diseases. ICAM-1 is a ligand for LFA-1(integrin). When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 interaction and then transmigrate into tissues. Presence with heavy glycosylation and other structural characteristics, ICAM-1 possesses binding sites for a number of immune-associated ligands and serves as the binding site for entry of the major group of human Rhinovirus (HRV) into various cell types. ICAM-1 also becomes known for its affinity for Plasmodium falciparum-infected erythrocytes (PFIE), providing more of a role in infectious disease. Previous studies have shown that ICAM-1 is involved in inflammatory reactions and that a defect in ICAM-1 gene inhibits allergic contact hypersensitivity.