Western Blotting (WB), Flow Cytometry (FACS), Immunofluorescence (IF)
Purpose
ESAM antibody
Specificity
Recombinant human ESAM
Characteristics
Chromosomal location: 11q24.2 Produced from sera of rabbits immunized with highly pure recombinant human soluble ESAM (Endothelial cell-selective adhesion molecule, Q30-A247, SwissProt: #Q96AP7) as the immunizing antigen.
Purification
Anti-human ESAM was purified by affinity chromatography with immobilized Protein A.
ESAM
Reactivity: Human
WB
Host: Rabbit
Polyclonal
unconjugated
Application Notes
Western Blot: Use 2-5 μg/mL
Restrictions
For Research Use only
Format
Lyophilized
Reconstitution
Centrifuge vial prior to opening. Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL.
Buffer
PBS
Handling Advice
Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.
Storage
4 °C,-20 °C
Storage Comment
The lyophilized antibody is stable for at least 2 years at -20°C. After sterile reconstitution the antibody is stable at 2-8°C for up to 6 months. Frozen aliquots are stable for at least 6 months when stored at -20°C. Addition of a carrier protein or 50% glycerol is recommended for frozen aliquots.
ESAM, W117m,Endothelial cell selective adhesion molecule (ESAM) is a 55 kDa type I transmembrane glycoprotein that belongs to the JAM family of immunoglobulin superfamily molecules. 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 hemophilic adhesion. In the cytoplasmic domain, there is a docking site for the multifunctional adaptor protein MAGI1. 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. ESAM deficient mice have no defect in vascularization but do have reduced angiogenic potential. This may be due to a decreased migratory response to FGF2.