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Validated All-in-One™ qPCR Primer for EPHB2(NM_017449.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
Ephrin receptors and their ligands, the ephrins, mediate numerous developmental processes, particularly in the nervous system. Based on their structures and sequence relationships, ephrins are divided into the ephrin-A (EFNA) class, which are anchored to the membrane by a glycosylphosphatidylinositol linkage, and the ephrin-B (EFNB) class, which are transmembrane proteins.
Gene References into function
- RYK, a catalytically inactive receptor tyrosine kinase, associates with EphB2 and EphB3 but does not interact with AF-6.
- role of extracellular signal-regulated kinase (ERK) during the differentiation of human monoblastic U937 cells stimulated by granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor (TNF)
- liganded to EFNB1 and EFNB2, expresssed in gastric cancer
- Glioma migration and invasion are promoted by activation of EphB2 or inhibited by blocking EphB2. Dysregulation of EphB2 expression or function may underlie glioma invasion.
- our findings suggest that mutational inactivation of EPHB2 may be important in the progression and metastasis of prostate cancer.
- defined the expression patterns of human ephrinB2, EphB4, and EphB2 in normal vessels of neonates (i.e. umbilici) and adults and compared them with those in congenital venous malformations
- analysis of EphB1, EphB2, and EphB4-binding peptides interaction with antagonists with ephrin-like affinity
- loss of EphB expression represents a critical step in colorectal cancer progression
- Deregulated EphB2 expression may play a role in several cancer types with loss of EphB2 expression serving as an indicator of the possible pathogenetic role of EphB2 signaling in the maintenance of tissue architecture of colon epithelium.
- progressive loss of EphB2 expression seen in each critical step of colon carcinogenesis, including the onset of invasion, dedifferentiation and metastasis which are paralleled by adverse patient outcome
- These results demonstrate that the MAPK ERK signaling pathway contributes to the p53-independent antiproliferative functions of p14ARF. Furthermore, they identify a new mechanism by which phosphorylation at serine 216 participates to Cdc25C inactivation.
- analysis of germline EPHB2 alterations in patients with colorectal tumors
- High EPHB2 mutation rate is associated with gastric tumors with microsatellite instability
- novel link between EphB forward signaling and SDF-1-induced signaling demonstrates a mechanism for cooperative regulation of endothelial cell movement.
- Notch signaling by induction of Dll1 was necessary & sufficient to regulate ephrin-B2 expression & induce ephrin-B2-dependent branching morphogenesis in human arterial EC.
- Genetic or epigenetic alterations of the EPHB2 gene might be an uncommon event in the development or progression of gastric cancers.
- In conclusion, alpha(2A)-adrenoreceptor activates ERK and Akt in intestinal cells by a common pathway which depends on PI3-kinase activation and results from EGF receptor transactivation.
- A tumor suppressor role for EPHB2 in rare colorectal cancer cases; rare germline EPHB2 variants may contribute to a small fraction of hereditary colorectal cancer.
- Overexpression of the EphA4 gene and reduced expression of the EphB2 gene may thus be a useful predictor of liver metastasis in patients with colorectal cancer.
- MMP7 and MMP9-mediated cleavage of EphB2 is induced by receptor-ligand interactions at the cell surface and that this event triggers cell-repulsive responses
