Recombinant Human Endothelial Cell Adhesion Molecule/ESAM (C-Fc)
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| Amount : | 50 µg |
| Content : | Lyophilized from a 0.2 µm filtered solution of 20mM PB,150mM NaCl,pH7.4. |
| AA sequence : | Recombinant Human ESAM is produced by our Mammalian expression system and the target gene encoding Gln30-Ala247 is expressed with a Fc tag at the C-terminus. |
| Alternative Name : | Endothelial Cell-Selective Adhesion Molecule, ESAM |
Source : Human Cells;
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. 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. ESAM is expressed on endothelial cells, activated platelets and megakaryocytes. The ECD of human and mouse ESAM share 69% amino acid identity.
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. 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. ESAM is expressed on endothelial cells, activated platelets and megakaryocytes. The ECD of human and mouse ESAM share 69% amino acid identity.
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