Human EphB4 Antibody Summary
Ala16-Ala539
Accession # AAH52804
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
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Detection of EphB4 in MCF‑7 Human Cell Line by Flow Cytometry. MCF‑7 human breast cancer cell line was stained with Rat Anti-Human EphB4 Monoclonal Antibody (Catalog # MAB3038, filled histogram) or isotype control antibody (Catalog # MAB005, open histogram), followed by Allophycocyanin-conjugated Anti-Rat IgG F(ab')2Secondary Antibody (Catalog # F0113).
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: EphB4
EphB4, also known as Htk, Myk1, Tyro11, and Mdk2, is a member of the Eph receptor tyrosine kinase family and binds Ephrin-B2. The A and B class Eph proteins have a common structural organization (1‑4). The human EphB4 cDNA encodes a 987 amino acid precursor that includes a 15 amino acid (aa) signal sequence, a 524 aa extracellular domain (ECD), a 21 aa transmembrane segment, and a 427 aa cytoplasmic domain (5). The ECD contains an N-terminal globular domain, a cysteine‑rich domain, and two fibronectin type III domains. The cytoplasmic domain contains a juxtamembrane motif with two tyrosine residues which are the major autophosphorylation sites, a kinase domain, and a conserved sterile alpha motif (SAM) (5). Activation of kinase activity occurs after membrane-bound or clustered ligand recognition and binding. The ECD of human EphB4 shares 89% aa sequence identity with mouse EphB4 and 42‑45% aa sequence identity with human EphB1, 2, and 3. EphB4 is expressed preferentially on venous endothelial cells (EC) and inhibits cell-cell adhesion, chemotaxis, and angiogenesis. Opposing effects are induced by signaling through Ephrin-B2 expressed on arterial EC: adhesion, endothelial cell migration, and vessel sprouting (6). EphB4 singaling contributes to new vascularization by guiding venous EC away from Ephrin-B2 expressing EC. Ephrin-B2 signaling induces arterial EC to migrate towards nascent EphB4 expressing vessels (6). The combination of forward signaling through EphB4 and reverse signaling through Ephrin-B2 promotes in vivo mammary tumor growth and tumor‑associated angiogenesis (7). EphB4 promotes the differentiation of megakaryocytic and erythroid progenitors but not granulocytic or monocytic progenitors (8, 9).
- Poliakov, A. et al. (2004) Dev. Cell 7:465.
- Surawska, H. et al. (2004) Cytokine Growth Factor Rev. 15:419.
- Pasquale, E.B. (2005) Nat. Rev. Mol. Cell Biol. 6:462.
- Davy, A. and P. Soriano (2005) Dev. Dyn. 232:1.
- Bennett, B.D. et al. (1994) J. Biol. Chem. 269:14211.
- Fuller, T. et al. (2003) J. Cell Sci. 116:2461.
- Noren, N.K. et al. (2004) Proc. Natl. Acad. Sci. 101:5583.
- Wang, Z. et al. (2002) Blood 99:2740.
- Inada, T. et al. (1997) Blood 89:2757.
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