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phosphorylation of mTOR through signaling by EphB3 is a potential mechanism of AZD4547 resistance in GC cells
FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1.
EZH2-mediated epigenetic suppression of EphB3 inhibits gastric cancer proliferation and metastasis by affecting E-cadherin and vimentin expression.
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/AKT and STAT3 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 and suggest that disabling EPHB3 signaling is an important aspect to eliminate a roadblock at the onset of EMT 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/RACK1/Akt signalling complex
Our work shows that EphB3 is consistently expressed by malignant T lymphocytes, most frequently in combination with EphB6, and that stimulation with their common ligands strongly suppresses Fas-induced apoptosis in these cells.
Data show that EphB receptors interact with E-cadherin and with the metalloproteinase ADAM10 at sites of adhesion.
EphB3 provides critical support to the development and progression of NSCLC by stimulating cell growth, migration, and survival.
Ephrin B3 receptor regulates the synthesis and release of D-serine in astrocytes, which may have important implications on synaptic transmission and plasticity.
RYK, a catalytically inactive receptor tyrosine kinase, associates with EphB2 and EphB3 but does not interact with AF-6.
while catalytic activity of EphB3 is required for inhibition of integrin-mediated cell adhesion, a distinct signaling pathway to Rho GTPases shared by WT- and KD-EphB3 receptor mediates inhibition of directional cell migration
EphB3-ephrin-B interaction promotes mesenchymal-to-epithelial transition (MET) by re-establishing epithelial cell-cell junctions and such an MET-promoting effect contributes to EphB3-mediated tumor suppression.
EPHB3, MASP1 and SST map to 3q26.2-q29 and may have roles in squamous cell carcinoma of the lung
although both EphB2 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-deficient thymuses
that EphB3 signaling plays a deleterious role in synaptic stability and plasticity after traumatic brain injury
Ephrin-B3 expression is localized to the lateral cortex extramodular zones in the developing inferior colliculus
Mule also regulates protein levels of the receptor tyrosine kinase 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 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 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.
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.
These results demonstrate that EphB receptors influence auditory cortical responses, and suggest that EphB signaling has multiple functions in auditory system development.
Data suggest that both EphB2 and EphB3 receptors are required coordinately for pancreatic development.
tumor suppressor p53 expression was increased following EphB3 stimulation and is reduced in the absence of either EphB3 or ephrinB3.
A trans-synaptic interaction between EphB2 in the presynaptic compartment and ephrin-B3 in the postsynaptic compartment regulates synapse density and the formation of dendritic spines.
Organ of Corti and spiral ganglion showed strong expression of EphA4, EphB3, ephrin-A3, ephrin-B2 and ephrin-B3. In lateral wall, EphA4, ephrin-A3 and ephrin-B2 were strongly expressed.
EphB1 and EphB3 receptor knockout mice exhibited significantly diminished DPOAE levels as compared to wild-type littermates, indicating that these specific Eph receptors are necessary for normal cochlear function.
RYK regulates cell migration during mammalian cortical development through the binding to Eph receptors
mutants of EphB2 and EphB3 receptor genes displayed a morphological defect in the ventral midbrain
Both reduction of EphB3 function in adult heterozygous animals and loss of function in homozygous animals greatly decreased RGC axon re-extension or sprouting after optic nerve injury.
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