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This study reported the identification of germline loss-of-function EPHB4 mutations in vein of Galen aneurysmal malformation.
knock-in of EPHB4 mutation in HEK293T cells also induced mTORC1 activity. Our data demonstrate the pathogenicity of the identified EPHB4 mutation as a novel cause of Central conducting lymphatic anomaly and suggesting that ERK inhibitors may have therapeutic benefits in such patients with complex lymphatic anomalies
miR-454 promotes the proliferation and invasion of trophoblast cells by inhibiting EPHB4 expression.
EphB4 expression is associated with colorectal cancer cell proliferation and vascularization.
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-DLL4/Notch-EphB4-Erk1/2 may provide an insight into mechanism of CCM3-ablation-mediated angiogenesis.
EphB4 overexpression is associated with resistance to dasatinib in chronic myeloid leukemia.
this study uncovered the character of EPHB4-regulating endothelial activation in the pathogenesis of preeclampsia
HOXA9 transcriptionally regulated EPHB4 expression to modulate trophoblasts migration and invasion, which may suggest a contribution of HOXA9-EPHB4 in the poor placentation in the pathogenesis of preeclampsia.
Inhibition of EphB4 forward signaling using soluble EphB4 protein fused with murine serum albumin 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) therapeutic target.
Study illustrates that aberrant activation of EphB4/ephrinB2 may mediate chronic myeloid leukemia resistance involved in cytoskeletal proteins.
both EphA2 and EphB4 show potential as target for image-guided colorectal cancer surgery, but EphB4 seems to have the best characteristics with respect to tumor/normal mucosa distribution.
Survival analysis showed that the non-small cell lung carcinoma patients with enhanced expression of CK7, ELF3, EGFR, and EphB4 mRNA in peripheral blood leukocytes had poorer disease-free survival and overall survival than those without.
Enhanced EphB4 expression was significantly associated with Thyroid Lesions.
LISA method may be considered rapid and sensitive enough to detect even low levels of total and phosphorylated EphB4 Cost-effectiveness of this method for the detection of differential expression of EphB4 proteins in clinics is also noticeable.
EphB4 facilitates stromal-mediated support of hematopoiesis in hematopoietic stem cells.
Inhibition of Akt1 function abolishes Eph-B-mediated venous remodeling suggesting that Eph-B4 regulates arteriovenous fistula venous adaptation through an Akt1-mediated mechanism.
ephrinB2/EphB4 signaling is a key regulator of intussusceptive angiogenesis; EphB4 does not affect VEGF-R2 activation or internalization, but regulates its downstream signaling through p-ERK1/2
Production of inflammatory cytokines was inhibited by Ti particles through bidirectional signals. Addition of ephB4Fc inhibited the osteoclastmediated formation of Ti particles via bidirectional ephrinB2/ephB4 signaling. Activation of this bidirectional signaling pathway may be a potential clinical treatment for osteolysis surrounding prostheses.
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 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 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 can be effectively compensated, most possibly by other ephrins with similar chemical structures
Eph-B4 stimulates eNOS phosphorylation in vitro and may mediate vein graft adaptation by regulation of eNOS activity in vivo.
Its overexpression causes cisplatin resistant in melanomas.
These data indicate that ephrinB2/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
EphB4-forward signaling plays a crucial role in the development of cardiac progenitor cells.
EPHB4 plays an essential role in regulating small artery contractility and blood pressure
the luminal epithelial EphB4 signaling contributes, most likely via wnt signaling, to the regulation of migration and cell fate of early progenitors and is involved in the determination of branching points along the mammary ductal tree
thymocytes develop normally in the absence of EPHB4, and T cells derived from EPHB4-deleted thymic epithelian cells have normal function.
These results are the first to identify EphB4 and its cross-talk with PDGFRbeta as unexpected vital determinants of tumor cell survival in alveolar rhabdomyosarcoma.
Identify EphB4 signaling as a pathway allowing podocytes to survive transient capillary collapse during glomerular disease.
Eph receptor gene ephb4b is highly expressed in dorsal forerunner cells (DFCs) whereas ephrin ligand genes, including efnb2b, 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