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These results indicated the suppressive effect of Form on colon carcinoma cell proliferation and invasion, possibly via miR149induced EphB3 downregulation and the inhibition of the PI3K (Montrer PIK3CA Protéines)/AKT (Montrer AKT1 Protéines) and STAT3 (Montrer STAT3 Protéines) signaling pathways.
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.
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 (Montrer SNAI1 Protéines) and suggest that disabling EPHB3 signaling is an important aspect to eliminate a roadblock at the onset of EMT (Montrer ITK Protéines) 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 (Montrer PPP2R4 Protéines)/RACK1 (Montrer GNB2L1 Protéines)/Akt (Montrer AKT1 Protéines) signalling complex
Our work shows that EphB3 is consistently expressed by malignant T lymphocytes, most frequently in combination with EphB6 (Montrer EPHB6 Protéines), and that stimulation with their common ligands strongly suppresses Fas (Montrer FAS Protéines)-induced apoptosis in these cells.
Data show that EphB receptors interact with E-cadherin (Montrer CDH1 Protéines) and with the metalloproteinase ADAM10 (Montrer ADAM10 Protéines) at sites of adhesion.
EphB3 provides critical support to the development and progression of NSCLC by stimulating cell growth, migration, and survival.
although both EphB2 (Montrer EPHB2 Protéines) and EphB3 are necessary for cortical thymic epithelial maturation, the relevance of EphB3 is greater since EphB3-/- thymic cortex exhibits a more severe phenotype than that of EphB2 (Montrer EPHB2 Protéines)-deficient thymuses
that EphB3 signaling plays a deleterious role in synaptic stability and plasticity after traumatic brain injury
Ephrin-B3 (Montrer EFNB3 Protéines) expression is localized to the lateral cortex extramodular zones in the developing inferior colliculus
Mule also regulates protein levels of the receptor tyrosine kinase (Montrer ERBB3 Protéines) 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 (Montrer EPHB2 Protéines) 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 (Montrer EPHB2 Protéines) and EphB3 are involved in the control of thymic epithelial cells (TEC (Montrer NR4A3 Protéines)) survival and that the absence of these molecules causes increased apoptotic TEC (Montrer NR4A3 Protéines).
EphB2 (Montrer EPHB2 Protéines) 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 (Montrer PPP2R2B Protéines)/RACK1 (Montrer GNB2L1 Protéines)/Akt (Montrer AKT1 Protéines) signalling complex
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