Data sheet
| Specificity | reactive with Human ICAM-1/CD54，reactivity with other related proteins not observed |
| Assay Range | 31.2-2000 pg/ml |
| Sensitivity | 7 pg/ml |
| Size | 96 Tests |
| Storage | 2-8℃ |
| Background | Intercellular adhesion molecule -1 (ICAM-1), also known as CD54 binding of leukocytes integration of LFA-1 and Mac-1. White blood cells, epithelial cells and resting endothelial cells, as well as some other types of cells on the expression of ICAM-1 is weak, but the expression can stimulate IFN-gamma, TNF-alpha, IL-1beta and LPS. The soluble ICAM-1 is the biologically active form in the serum, which may be due from the cell surface proteolytic cutting. |
| Assay principle | This Human ICAM-1/CD54 ELISA Kit was based on standard sandwich enzyme-linked immunosorbent assay technology. Human ICAM-1/CD54 specific antibodies were precoated onto 96-well plates. The Human ICAM-1/CD54 specific detection antibodies were biotinylated. The test samples and biotinylated detection antibodies were added to the wells subsequently and then followed by washing the plate. Streptavidin-HRP was added and unbound conjugates were washed away with wash buffer. HRP substrate TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow color is proportional to the Human ICAM-1/CD54 amount of sample captured in plate. |
| Sample type | serum，plasma，cell culture supernatant |
| Assay duration | 4 hours |
| Assay format | Sandwich |
| Alternative Name of Analyte | Intercellular Adhesion Molecule 1；BB2；CD54；P3.58 |
More info
ICAM1 (Inter-Cellular Adhesion Molecule 1), also known as CD54, is a type of intercellular adhesion molecule. It is a cell surface glycoprotein which is typically expressed onendothelial cells and cells of the immune system. It binds to integrins of typeCD11a / CD18, or CD11b / CD18 and is also exploited by rhinovirus as a receptor.Its expression is activated by p53 in an NF-kappaB-independent manner and induced by TNFalpha in a process that involves IKK beta.