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showed that patients with SSc (show CYP11A1 ELISA Kits) or SLE have AAb against EphB2, a protein involved in angiogenesis, and THEX1 (show ERI1 ELISA Kits), 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 (show SNAI1 ELISA Kits) - an inducer of epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)) - is anti-correlated in colorectal cancer cell lines and tumors
Tiam2 (show TIAM2 ELISA Kits)/Rac (show AKT1 ELISA Kits) are key components of EphB2 trans-endocytosis and are important for cell repulsion.
High expression of junctional adhesion molecule-A (show F11R ELISA Kits) 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 (show PIK3CA ELISA Kits))/Akt (show AKT1 ELISA Kits) protein-mediated glycogen synthase kinase-3beta (GSK-3beta (show GSK3b ELISA Kits)) inhibition.
Expression of the Receptor Tyrosine Kinase (show RET ELISA Kits) EphB2 on Dendritic Cells Is Modulated by Toll (show TLR4 ELISA Kits)-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 (show EFNB1 ELISA Kits) were invoked in dental pulp stem cells with TNF-alpha (show TNF ELISA Kits) treatment via the JNK (show MAPK8 ELISA Kits)-dependent pathway, but not NF-kB, p38 MAPK (show MAPK14 ELISA Kits) or MEK (show MAP2K1 ELISA Kits) signalling.
The results show an intricate interplay between p53 (show TP53 ELISA Kits) and TGF-beta3 (show TGFB3 ELISA Kits) whereby p53 (show TP53 ELISA Kits) inhibits the TGF-beta3 (show TGFB3 ELISA Kits)-induced expression of genes, e.g., EPHB2, to impede tumor cell invasion and migration
ephrin B3 (show EFNB3 ELISA Kits)/EphB2 are obvious candidates for driving the Syk (show SYK ELISA Kits)-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 (show ERBB3 ELISA Kits), 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 (show ADD3 ELISA Kits) interaction.
EphB4 (show EPHB4 ELISA Kits) plays an irreplaceable role in bone regeneration in an inflammatory microenvironment, whereas the functional loss of ephrinB2 (show EFNB2 ELISA Kits) 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 (show EPHB1 ELISA Kits)/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 (show EFNB1 ELISA Kits) 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 (show GRIN1 ELISA Kits) requiring the PDZ (show INADL ELISA Kits)-binding motif of EphB2.
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