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Study found up-regulated expression of ephrinB3/EphB3 in intractable temporal lobe epilepsy patients and experimental temporal lobe epilepsy rats, which suggested that ephrinB3/EphB3 might be involved in the pathogenesis of temporal lobe epilepsy
work suggested that EphB3 acted as a tumor promoter in Papillary Thyroid Cancer by increasing the in vitro migration as well as the in vivo metastasis of Papillary Thyroid Cancer cells through regulating the activities of Vav2 and Rho GTPases in a kinase-dependent manner.
knockdown expression of EphB3 could suppress cell proliferation and invasion, and ectopic expression of EphB3 restored the phenotypes of colonic carcinoma cell lines transfected with miR149. In addition, silencing of EphB3 significantly affected cycle progression distribution and increased apoptosis in colonic carcinoma cell lines.
These results show that EphB3 protein is lost in ovarian serous carcinoma and is associated with tumor grade and FIGO stage, which indicate that EphB3 protein may play a role in carcinogenesis of ovarian serous carcinoma and may be used as a molecular marker for prognosis.
results identify EPHB3 as a novel target of SNAIL1 (show SNAI1 Proteins) and suggest that disabling EPHB3 signaling is an important aspect to eliminate a roadblock at the onset of EMT (show ITK Proteins) processes.
These results uncover enhancer decommissioning as a mechanism for transcriptional silencing of the EPHB3 tumor suppressor.
EphB3 suppresses non-small-cell lung cancer metastasis via a PP2A (show PPP2R4 Proteins)/RACK1 (show GNB2L1 Proteins)/Akt (show AKT1 Proteins) signalling complex
Our work shows that EphB3 is consistently expressed by malignant T lymphocytes, most frequently in combination with EphB6 (show EPHB6 Proteins), and that stimulation with their common ligands strongly suppresses Fas (show FAS Proteins)-induced apoptosis in these cells.
Data show that EphB receptors interact with E-cadherin (show CDH1 Proteins) and with the metalloproteinase ADAM10 (show ADAM10 Proteins) at sites of adhesion.
EphB3 provides critical support to the development and progression of NSCLC by stimulating cell growth, migration, and survival.
Mule also regulates protein levels of the receptor tyrosine kinase (show ERBB3 Proteins) EphB3 by targeting it for proteasomal and lysosomal degradation.
A novel dependence receptor role of EphB3 in oligodendrocyte cell death after spinal cord injury.
These results suggest a major function for forward signaling through EphB2 (show EPHB2 Proteins) and, to a lesser extent, EphB3, in either colonizing progenitor cells or thymic stromal cells.
Conclude that EphB3 mediates cell death in the adult cortex through a novel dependence receptor-mediated cell death mechanism in the injured adult cortex and is attenuated following ephrinB3 stimulation.
EphB2 and EphB3 are involved in the control of thymic epithelial cells (TEC) survival and that the absence of these molecules causes increased apoptotic TEC.
EphB2 (show EPHB2 Proteins) and EphB3 reverse signaling are critical for the normal development of the projection from the ventral cochlear nucleus to the contralateral medial nucleus of the trapezoid body.
EphB3 suppresses non-small-cell lung cancer metastasis via a PP2A (show PPP2R2B Proteins)/RACK1 (show GNB2L1 Proteins)/Akt (show AKT1 Proteins) signalling complex
EphB-deficient SCID chimeras show profoundly altered thymic epithelial organization that confirms a significant role for EphB2 and EphB3 receptors in the thymocyte-TEC crosstalk.
Data suggest that both EphB2 (show EPHB2 Proteins) and EphB3 receptors are required coordinately for pancreatic development.
tumor suppressor p53 (show TP53 Proteins) expression was increased following EphB3 stimulation and is reduced in the absence of either EphB3 or ephrinB3.
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. The Eph family of receptors are divided into two groups based on the similarity of their extracellular domain sequences and their affinities for binding ephrin-A and ephrin-B ligands. Ephrin receptors make up the largest subgroup of the receptor tyrosine kinase (RTK) family. This gene encodes a receptor for ephrin-B family members.
ephrin receptor EphB3
, EPH receptor B3
, ephrin receptor EphB3-like
, ephrin type-B receptor 3-like
, EPH-like kinase 2
, EPH-like tyrosine kinase 2
, EPH-like tyrosine kinase-2
, embryonic kinase 2
, ephrin type-B receptor 3
, human embryo kinase 2
, tyrosine-protein kinase TYRO6
, developmental kinase 5
, tyrosine-protein kinase receptor SEK-4
, EPH-like kinase 10
, eph-like kinase 3
, eph-like receptor tyrosine kinase 3
, tyrosine-protein kinase receptor ZEK3
, tyrosine-protein kinase receptor TCK