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functional expression of EphB4 is considered a promising differentiating characteristic, preferentially determined by non-invasive in vivo imaging, which may improve personalized theranostics of malignant melanoma.
The identified endothelial signalling pathway of CCM3 (show PDCD10 Proteins)-DLL4 (show DLL4 Proteins)/Notch (show NOTCH1 Proteins)-EphB4-Erk1/2 may provide an insight into mechanism of CCM3 (show PDCD10 Proteins)-ablation-mediated angiogenesis.
EphB4 overexpression is associated with resistance to dasatinib in chronic myeloid leukemia (show BCL11A Proteins).
this study uncovered the character of EPHB4-regulating endothelial activation in the pathogenesis of preeclampsia
HOXA9 (show HOXA9 Proteins) transcriptionally regulated EPHB4 expression to modulate trophoblasts migration and invasion, which may suggest a contribution of HOXA9 (show HOXA9 Proteins)-EPHB4 in the poor placentation in the pathogenesis of preeclampsia.
Inhibition of EphB4 forward signaling using soluble EphB4 protein fused (show AXIN1 Proteins) with murine serum albumin (show ALB Proteins) failed to affect eRMS model tumor progression, but did moderately slow progression in murine aRMS
EPHB4 mutations were identified in patients with multifocal capillary malformation with arteriovenous malformations.
EPHB4 is a critical regulator of early lymphatic vascular development; mutations in the gene can cause an autosomal dominant form of lymphatic-related hydrops fetalis that is associated with a high mortality rate
The expression of EPHB4 was increased in gastric cancer and increased EPHB4 expression was correlated with poor survival. Knockdown of EPHB4 promoted adhesion and exerted diverse effects on migration of gastric cancer cells.
EphB4 protein acts as a tumour promoter associated with proliferation, invasion, and angiogenesis, and may be used as a potential colorectal cancer (CRC (show CALR Proteins)) therapeutic target.
These findings implicate a molecular disinhibitory mechanism driving the establishment of perisomatic inhibition whereby visual experience enhances Pten signalling, resulting in the suppression of EphB4 expression; this relieves a native synaptic repulsion between PV cells and pyramidal neurons, thereby promoting the assembly of perisomatic inhibition.
As endothelial progenitor cells (EPCs)derived from mouse bone marrow were cultured on substrates of increasing stiffness, the mRNA and protein levels of the specific arterial endothelial cell marker ephrinB2 (show EFNB2 Proteins) were found to increase, while the expression of the venous marker EphB4 decreased
EPHB4 is a critical regulator of early lymphatic vascular development; mutations in the gene can cause an autosomal dominant form of LRHF that is associated with a high mortality rate
These results identify EPHB4/ephrin B2 (show EFNB2 Proteins) signaling as critical to Hematopoietic stem and progenitor cells mobilization from bone marrow
EphB4 plays an irreplaceable role in bone regeneration in an inflammatory microenvironment, whereas the functional loss of ephrinB2 (show EFNB2 Proteins) can be effectively compensated, most possibly by other ephrins with similar chemical structures
Eph (show EPHA1 Proteins)-B4 stimulates eNOS (show NOS3 Proteins) phosphorylation in vitro and may mediate vein graft adaptation by regulation of eNOS (show NOS3 Proteins) activity in vivo.
These data indicate that ephrinB2 (show EFNB2 Proteins)/EphB4 signaling within the osteoblast lineage is required for late stages of osteoblast differentiation.
EphB4 promotes endochondral ossification while inhibiting osteoclast development during callus formation.
Selective inhibition of EphB4 using a functional blocking antibody results in defective lymphatic valve development.
Overexpression of bone-specific Ephb4 clearly demonstrated prevention of the development and/or progression of fibrosis in OA synovial membrane
Eph (show EPHA1 Proteins) receptor gene ephb4b is highly expressed in dorsal forerunner cells (DFCs) whereas ephrin ligand genes, including efnb2b (show EFNB2 Proteins), are expressed in cells next to the DFC cluster during zebrafish gastrulation.
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 binds to ephrin-B2 and plays an essential role in vascular development.
ephrin receptor EphB4
, ephrin type-B receptor 4
, hepatoma transmembrane kinase
, soluble EPHB4 variant 1
, soluble EPHB4 variant 2
, soluble EPHB4 variant 3
, tyrosine-protein kinase TYRO11
, tyrosine-protein kinase receptor HTK
, EPH receptor B4
, eph receptor tyrosine kinase
, ephrin type-B receptor 4-like
, developmental kinase 2
, tyrosine kinase MYK-1
, eph receptor B4b
, eph-like receptor tyrosine kinase 8