This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 51.4 kDa. The protein migrates as 60-100 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 1.0 EU per μg by the LAL method.
>95% as determined by SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
Contact us for customized product form or formulation.
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
No activity loss is observed after storage at:
4-8°C for 12 months in lyophilized state;
-70°C for 3 months under sterile conditions after reconstitution.
Human ICAM-1, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.
Inter-Cellular Adhesion Molecule 1 (ICAM-1) is also known as Cluster of Differentiation 54 (CD54), is a member of the immunoglobulin superfamily, and is a cell surface glycoprotein which is typically expressed in low concentrations on endothelial cells and cells of the immune system. The protein encoded by this gene is a type of intercellular adhesion molecule continuously present in low concentrations in the membranes of leukocytes and endothelial cells. Upon cytokine stimulation, the concentrations greatly increase. ICAM-1 can be induced by interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFα) and is expressed by the vascular endothelium, macrophages, and lymphocytes. ICAM-1 is a ligand for LFA-1 (integrin), a receptor found on leukocytes. When activated, leukocytes bind to endothelial cells via ICAM-1/LFA-1 and then transmigrate into tissues. ICAM-1 has been implicated in subarachnoid hemorrhage (SAH). Levels of ICAM-1 are shown to be significantly elevated in patients with SAH over control subjects in many studies. ICAM-1 expressed by respiratory epithelial cells is also the binding site for rhinovirus, the causative agent of most common colds.