Purity
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain
Endotoxin Level
<0.01 EU per 1 μg of the protein by the LAL method.
Activity
Measured by its ability to induce ERK phosphorylation in BaF3 mouse pro‑B cells transfected with human ESAM. Stimulation of 2.5 x 10 5 serum-starved hESAM transfected BaF3 cells with 25 µg Recombinant Human ESAM Fc Chimera (Catalog # ) for 30 minutes at 37° C leads to ERK phosphorylation.
Source
Mouse myeloma cell line, NS0-derived
Human ESAM
(Gln30 - Ala247)
Accession # Q96AP7IEGRMD Human IgG1
(Pro100 - Lys330)N-terminus C-terminus Accession #
N-terminal Sequence
AnalysisNo results obtained: Gln30 predicted
Predicted Molecular Mass
50.3 kDa (monomer)
SDS-PAGE
67-75 kDa, reducing conditions
2688-EC |
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Formulation Lyophilized from a 0.2 μm filtered solution in PBS. | ||
Reconstitution Reconstitute at 100 μg/mL in sterile PBS. | ||
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. | ||
Stability & Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Background: ESAM
Endothelial cell-selective adhesion molecule (ESAM) is a 55 kDa type I transmembrane glycoprotein that belongs to the JAM family of immunoglobulin superfamily molecules (1, 2). Human ESAM is synthesized as a 390 amino acid (aa) protein composed of a 29 aa signal peptide, a 216 aa extracellular region, a putative 26 aa transmembrane segment, and a 119 aa cytoplasmic domain. The extracellular region contains one V-type and one C2-type Ig domain and is involved in homophilic adhesion (1). In the cytoplasmic domain, there is a docking site for the multifunctional adaptor protein MAGI-1 (3). The extracellular region of human ESAM shows 90%, 74%, 69% and 67% aa identity with monkey, canine, mouse and rat extracellular ESAM, respectively. ESAM is expressed on endothelial cells, activated platelets and megakaryocytes, and can be found associated with cell-to-cell junctions. Whether ESAM is restricted to a particular junctional type is not clear (1, 2). ESAM deficient mice have no defect in vascularization but do have reduced angiogenic potential. This may be due to a decreased migratory response to FGF-2 (4).
References:
Hirata, K-I, et al. (2001) J. Biol. Chem. 276:16223.
Nasdala, I. et al. (2002) J. Biol. Chem. 277:16294.
Wegmann, F. et al. (2004) Exp. Cell Res. 300:121.
Ishida, T. et. al. (2003) J. Biol. Chem. 278:34598.
Long Name:
Endothelial Cell Adhesion Molecule
Entrez Gene IDs:
90952 (Human); 69524 (Mouse)
Alternate Names:
2310008D05Rik; endothelial cell adhesion molecule; endothelial cell-selective adhesion molecule; ESAM; HUEL (C4orf1)-interacting protein; LP4791 protein; W117m
