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Recombinant Human ESAM Protein (aa 30-247, Fc Tag)
SKU: PKSH032380-50
Recombinant Human ESAM Protein (aa 30-247, Fc Tag)
| SKU # | PKSH032380 |
| Expression Host | HEK293 Cells |
Description
| Synonyms | ESAM, Endothelial Cell-Selective Adhesion Molecule |
| Species | Human |
| Expression Host | HEK293 Cells |
| Sequence | Gln30-Ala247 |
| Accession | Q96AP7 |
| Calculated Molecular Weight | 50.8 kDa |
| Observed Molecular Weight | 60-80 kDa |
| Tag | C-Fc |
| Bio-activity | Not validated for activity |
Properties
| Purity | > 95 % as determined by reducing SDS-PAGE. |
| Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method. |
| 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 a 0.2 μm filtered solution of 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 | Please refer to the printed manual for detailed information. |
Background
Endothelial Cell Adhesion Molecule (ESAM) is a 55 kDa type I transmembrane glycoprotein member of the JAM family of immunoglobulin superfamily molecules. The 390 amino acid Human ESAM contains a 216 amino acid extracellular domain (ECD) with a V-type and a C2-type immunoglobulin (Ig) domain. The ECD of human and mouse ESAM share 69% amino acid identity. ESAM is specifically expressed at endothelial tight junctions and on activated platelets and performs homophilic adhesion activity. The adaptor protein membrane-associated guanylate kinase MAGI-1 has been identified as an intracellular binding partner of ESAM. In addition; ESAM at endothelial tight junctions participates in the migration of neutrophils through the vessel wall; possibly by influencing endothelial cell contacts. ESAM-deficient mice were described with lowered angiogenic potential; and accordingly; overexpression of ESAM is closely associated with certain tumor growth and metastasis.