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The data further showed that mitochondrial fission significantly promoted the reprogramming of focal-adhesion dynamics and lamellipodia formation in hepatocellular carcinoma cells mainly by activating typical Ca(2+) /CaMKII/ERK/FAK pathway.
These findings suggested that miR-204 might serve as a tumor suppressor in the development of cervical cancer by directly targeting EphB2.
EphB2 signaling-mediated Sirt3 expression reduces MSC senescence by maintaining mitochondrial reactive oxygen species homeostasis.
This study showed that EphB2 cells have a transient increase in migration after heterotypic activation, which underlies a shift in the EphB2-ephrinB1 border but is not required for segregation or border sharpening.
This is the first study to link SLC1A3 and EPHB2 to clinically relevant vertebral osteoporosis phenotypes.
Data show that EPHB2 predicted poor breast cancer survival and EPHB2 protein expression has also prognostic value depending on cell localization.
showed that patients with SSc or SLE have AAb against EphB2, a protein involved in angiogenesis, and THEX1, a 3'-5' exoribonuclease involved in histone mRNA degradation. We have further identified a peptide from EphB2 as a specific and sensitive tool for SLE diagnosis
show that expression of EPHB2 and SNAIL1 - an inducer of epithelial-mesenchymal transition (EMT) - is anti-correlated in colorectal cancer cell lines and tumors
Tiam2/Rac are key components of EphB2 trans-endocytosis and are important for cell repulsion.
High expression of junctional adhesion molecule-A and EphB2 can predict poor overall survival and high mortality rate, and EphB2 is an independent prognostic biomarker in lung adenocarcinoma patients.
Data show that activation of EphB2 receptor kinase arrests tau protein hyperphosphorylation through phosphatidylinositol 3-kinase (PI3K)/Akt protein-mediated glycogen synthase kinase-3beta (GSK-3beta) inhibition.
Expression of the Receptor Tyrosine Kinase EphB2 on Dendritic Cells Is Modulated by Toll-Like Receptor Ligation but Is Not Required for T Cell Activation
Myosin 1 functions as an effector of EphB2/ephrinB signaling, controls cell morphology, and thereby cell repulsion.
EphB2 activation is required for ependymoma development as well as it inhibits differentiation and promotes proliferation of the transformed cell.
EphB2/ephrin-B1 were invoked in dental pulp stem cells with TNF-alpha treatment via the JNK-dependent pathway, but not NF-kB, p38 MAPK or MEK signalling.
The results show an intricate interplay between p53 and TGF-beta3 whereby p53 inhibits the TGF-beta3-induced expression of genes, e.g., EPHB2, to impede tumor cell invasion and migration
loss of EphB2 and gain of EphB4 expression represents an inflection point in the development, growth and possibly progression of TCC.
knockdown impairs monocyte transmigration through the endothelium
Data indicate that the Eph tyrosine kinase receptors EphB2 and EphA2 are involved in factor/coagulation factor VIIa (TF/FVIIa) signaling.
the upregulation of EphB2 receptors and its specific ligands leads to cholangiocarcinoma metastasis.
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
ephrin-B2 and EphA4 have graded and modular expression patterns in the developing inferior colliculus
Overexpression of EphB2 also rescued the ADDLs-induced depletion of the expression of EphB2 and GluN2B-containing NMDA receptors trafficking in cultured hippocampal neurons.
ephrin B3/EphB2 are obvious candidates for driving the Syk-dependent repulsive response.
The results of this study indicated that the decrease in spine density in the mPFC was associated with susceptibility to stress, and EphB2 downregulation in the mPFC increased the vulnerability to stress.
We here identify that EphB2 receptor tyrosine kinase, which is specifically expressed in glutamatergic neurons, is required for the innate fear responses in the neonatal brain.
Here, we identified the interaction sites of the EphB2 FN domain with ADDLs for the first time to develop a small (10 aa) peptide (Pep63) capable of blocking the EphB2-ADDL interaction.
EphB4 plays an irreplaceable role in bone regeneration in an inflammatory microenvironment, whereas the functional loss of ephrinB2 can be effectively compensated, most possibly by other ephrins with similar chemical structures
Authors suggest that aging is accompanied by the upregulation of miR-204 in the hippocampus, which downregulates EphB2 and results in reduced surface and total NR1 expression.
Findings suggest that a combination of forward and reverse EphB1/2 receptor-mediated signaling contribute to posterior branch of the anterior commissure and corpus callosum axon guidance
Results demonstrate that EphB2 reverse signaling plays a unique and requisite role in inhibiting the development of opiate-dependent tolerance in vivo
During re-epithelialization ephrin-B1 and its receptor EphB2 are both upregulated in vivo, just for the duration of repair.
EphB2 prevents amyloid-beta-induced depletion of cell surface GluN1 requiring the PDZ-binding motif of EphB2.
the unique cross-subclass interaction of EphB2 with ephrin A5 has evolved to function upstream of JNK signaling for the purpose of maintaining an adequate pool of progenitor cells to ensure proper closure of the optic fissure.
Study concludes that EphB2 forward signaling is required for long-term contextual fear conditioning memory formation.
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.
These findings connect the EphB signaling pathway to the regulation of intestinal adenoma initiation via Abl kinase.
These findings provide mechanistic evidence for the role of EphB2 in the early progression of cSCC to the invasive stage and identify EphB2 as a putative therapeutic target in this invasive skin cancer.
these data demonstrate that EphB2 signaling not only modulates platelet function within a thrombus but is also involved in the regulation of the function of isolated platelets in a contact-independent manner.
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 2 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. The protein encoded by this gene is a receptor for ephrin-B family members.
ephrin receptor EphB2
, EPH receptor B2
, ephrin type-B receptor 2-like
, EPH-like kinase 5
, developmentally-regulated Eph-related tyrosine kinase
, elk-related tyrosine kinase
, eph tyrosine kinase 3
, ephrin type-B receptor 2
, protein-tyrosine kinase HEK5
, renal carcinoma antigen NY-REN-47
, tyrosine-protein kinase TYRO5
, tyrosine-protein kinase receptor EPH-3
, neural kinase
, nuk receptor tyrosine kinase
, tyrosine-protein kinase receptor SEK-3
, embryo kinase 5 protein CEK5