Recombinant Human VCAM-1/CD106 Protein (His tag)
SKU: PDMH100116-100
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Recombinant Human VCAM-1/CD106 Protein (His tag)
SKU # | PDMH100116 |
Expression Host | HEK293 Cells |
Description
Synonyms | CD106, INCAM-100, L1CAM, V-CAM 1, VCAM-1, VCAM1, Vascular Cell Adhesion Protein 1 |
Species | Human |
Expression Host | HEK293 Cells |
Sequence | Phe25-Glu698 |
Accession | P19320 |
Calculated Molecular Weight | 76.7 kDa |
Observed Molecular Weight | 100 kDa |
Tag | C-His |
Bio-activity | Not validated for activity |
Properties
Purity | > 95% as determined by reducing SDS-PAGE. |
Endotoxin | Please contact us for more information. |
Storage | Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months. |
Shipping | This product is provided as lyophilized powder which is shipped with ice packs. |
Formulation | Lyophilized from sterile PBS, pH 7.4. Normally 5%-8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the printed manual. |
Reconstitution | It is recommended that sterile water be added to the vial to prepare a stock solution of 0.5 mg/mL. Concentration is measured by UV-Vis. |
Background
VCAM-1 is a single-pass type I membrane protein, contains 7 Ig-like C2-type domains. It is an endothelial ligand for very late antigen-4 (VLA-4) and α4β7 integrin expressed on leukocytes, and thus mediates leukocyte-endothelial cell adhesion and signal transduction. VCAM-1 expression is induced on endothelial cells during inflammatory bowel disease, atherosclerosis, allograft rejection, infection, and asthmatic responses. During these responses, VCAM-1 forms a scaffold for leukocyte migration. VCAM-1 also activates signals within endothelial cells resulting in the opening of an "endothelial cell gate" through which leukocytes migrate. VCAM-1 has been identified as a potential anti-inflammatory therapeutic target, the hypothesis being that reduced expression of VCAM-1 will slow the development of atherosclerosis. In addition, VCAM-1-activated signals in endothelial cells are regulated by cytokines indicating that it is important to consider both endothelial cell adhesion molecule expression and function during inflammatory processes.