详细说明
- Species ReactivityHuman
- SpecificityDetects human EphB4 in direct ELISAs and Western blots. In direct ELISAs and Western blots, no cross-reactivity with recombinant human EphA1, A2, A5, A6, A10, B2, B3, B6, recombinant mouse EphA3, A4, or recombinant rat EphB1 is observed.
- SourceMonoclonal Rat IgG1 Clone # 395810
- ImmunogenMouse myeloma cell line NS0-derived recombinant human EphB4
Ala16-Ala539
Accession # AAH52804 - FormulationSupplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.
- LabelAlexa Fluor 350
- Recommended
ConcentrationSample
- Flow Cytometry0.25-1 µg/10 6 cellsMCF‑7 human breast cancer cell line
- ShippingThe product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
- Stability & StorageStore the unopened product at 2 - 8 °C. Do not use past expiration date.
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).
- References:
- 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.
- Long Name:Eph Receptor B4
- Entrez Gene IDs:2050 (Human); 13846 (Mouse)
- Alternate Names:EC 2.7.10; EC 2.7.10.1; EPH receptor B4; EphB4; ephrin type-B receptor 4; hepatoma transmembrane kinase; Htk; HTKephrin receptor EphB4; Mdk2; Myk1; soluble EPHB4 variant 1; soluble EPHB4 variant 2; soluble EPHB4 variant 3; Tyro11; Tyrosine-protein kinase receptor HTK; Tyrosine-protein kinase TYRO11