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Lymphomas with low UTX expression express high levels of Efnb1, and cause significantly poor survival.
that expression of EFNB1 and EFNB2 is implicated in Th cell differentiation and migration to inflammatory sites in both EAE and MS
germinal center (GC)-expressed ephrin B1 (EFNB1) repulsively inhibited T cell to B cell adhesion and GC follicular T helper retention by signaling through TFH-expressed EPHB6 receptor; at the same time, EFNB1 promoted interleukin-21 production from GC TFH cells by signaling predominantly through EPHB4
these observations demonstrate the importance of ephrinB1 signalling between cells of the skeleton required for endochondral ossification.
an autonomous receptor-like role for ephrin-B reverse signaling in the tangential migration of interneurons into the neocortex using ephrin-B (EfnB1/B2/B3) conditional triple mutant (TM(lz)) mice, is reported.
These results indicate a novel mechanism of ephrin-Eph signaling independent of direct cell contact and proteolytic cleavage and suggest the participation of EphB2(+) extracellular vesicles in neural development and synapse physiology.
ephrin-B1-mediated cell segregation occurs in the early neuroepithelium.
Results suggest the involvement of ephrin-B1 signaling in astrocyte-mediated remodeling of excitatory synapses following injury, which can be accomplished through ephrin-B1-mediated regulation of STAT3 signaling in astrocytes.
Conditioned deletion of ephrinB1 and/or ephrinB2 in either thymocytes or thymic epithelial cells alters the organization of thymic medulla and favors the appearance of thymic epithelial cysts.
Efnb1 and Efnb2 in T cells are essential for pathogenic antibody production and for T cell migration to the inflamed paws in mice with collagen-induced arthritis.
The EphB2 and ephrin-B1 are possibly involved in epithelial boundary formation at the squamocolumnar junction.
EFNB1 contributes to the suppression of adipose inflammatory response. In obesity, reduction of adipose EFNB1 may accelerate the vicious cycle involved in adipose tissue inflammation.
Overexpression of ephrin B1 in bone cells enhances bone mass.
These results highlight the complex role of Eph:ephrin signaling in the development of the sensory-motor circuit innervating the limb.
The results of this study demonstrated that ephrin-B1 inhibits nonradial migration of pyramidal neurons, thereby controlling the pattern of cortical columns.
Ephrin-B1 and ephrin-B2 expressed on thymocytes play an autonomous role in T cell development and, expressed on thymic epithelial cells (TECs), their nonautonomous roles are partially overlapping.
Results show that Efnb1 is a negative regulator of smooth muscle cell (VSMC)contractility and blood pressure (BP).
myeloid lineage produced ephrin B1 is a negative regulator of bone resorption
the function of EFNB1 in the T cell compartment could be compensated by other members of the EFN family, and that such redundancy safeguards the pivotal roles of EFNB1 in T cell development and function.
Ephrin-B1 is necessary for cardiac tissue architecture cohesion by stabilizing the adult cardiomyocytes morphology through regulation of its lateral membrane.
bidirectional signaling between EphrinB1 and EphB3b coordinates the movements of the hepatic endoderm and adjacent lateral plate mesoderm (LPM), resulting in asymmetric positioning of the zebrafish liver.
Pathogenic or likely pathogenic variants in non-FGFR genes were identified in 43 individuals, with diagnostic yields of 14% and 15% in retrospective and prospective cohorts, respectively. Variants were identified most frequently in TCF12 (N = 22) and EFNB1 (N = 8), typically in individuals with nonsyndromic coronal craniosynostosis or TWIST1-negative clinically suspected Saethre-Chotzen syndrome.
Chronic hypoxia-induced slug promotes invasive behavior of prostate cancer cells by activating the expression of ephrin-B1.
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.
we demonstrate that mosaicism for EPHRIN-B1 expression induced by random X inactivation in heterozygous females results in robust cell segregation in human neuroepithelial cells, thus supplying experimental evidence that Eph/ephrin-mediated cell segregation is relevant to pathogenesis in human CFNS patients.
one novel (IVS2+3G>T) and one previously reported mutation (p.Gly151Ser) in EFNB1 Both patients were de novo cases without a family history of Craniofrontonasal syndrome.
While ephrin-B1 deficiency leads to abnormal visual pathways in mice, it leaves the human visual system, apart from deficits in binocular vision, largely normal.
that EphrinB1 (EFNB1) co-localizes with microtubules (MTs) during all phases of the cell cycle.
we report a family with a G151S mutation in the EFNB1 gene. The mutation was identified in two severely affected sisters and paradoxically in their clinically unaffected father.
T cells from rheumatoid arthritis (RA) patients expressed higher EFNB1 mRNA levels, which correlated with RA symptoms and laboratory findings. Expression of EFNB1 in T cells might be a parameter for monitoring RA disease activity and treatment responses.
Results indicate that EphrinB1 is uniquely dysregulated in medulloblastoma and promotes oncogenic responses in medulloblastoma cells, implicating ephrinB1 as a potential target
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.
Patients with EFNB1 mutations have a clear phenotype. This study will facilitate genetic counseling of parents and patients, and contribute to the diagnostic and screening process of patients with suspected CFNS.
CNK1 mediates ephrinB1 signaling that promotes cell migration through RhoA and JNK activity.
EphrinB1 expression is related to the metastasis of breast cancer and its enhanced expression confers a poor prognosis, suggesting that EphrinB1 may be a relevant therapeutic target in breast cancers.
High EFNB1 expression is associated with squamous cell carcinomas of the head and neck.
we report the identification of mosaic EFNB1 mutations in every individual with craniofrontonasal syndrome, confirming the suggested diagnosis and supporting the hypothesis of cellular interference in humans.
These results indicate a novel function of Nm23-H1 to control contact inhibition of locomotion, and its negative regulation by ephrin-B1.
Data show that EphrinB1, a PTPN13 substrate, interacts with ErbB2, and Src kinase mediates EphrinB1 phosphorylation and subsequent MAP Kinase signaling.
interactions between Smurfs and ephrinB1 regulates the maintenance of tissue boundaries through the control of ephrinB protein levels
Results identify the transcriptional co-repressor xTLE1/Groucho as an EphrinB1 interacting protein.
Ephrin-B1 and Wnt3A signaling contribute to region-specific neuronal plasticity in the developing optic tectum.
Tyrosine-298 in ephrin B1 is required for binding Grb4.
EphrinB1 reverse signaling is required to promote cellular movements into the eye field, and can rescue the FGF receptor-induced repression of retinal fate. respectively.
Gain- and loss-of-function experiments suggest that Xdsh associates with ephrinB1 and mediates ephrinB1 signalling through downstream members of the PCP pathway during eye field formation.
recruitment of STAT3 to ephrinB1, and its resulting Jak2-dependent activation and transcription of reporter targets, reveals a signaling pathway from ephrinB1 to the nucle
ephrinB1 associates with the Par polarity complex protein Par-6 and can compete with the small GTPase Cdc42 for association with Par-6.
Data demonstrate that phosphorylation of tyrosines 324 and 325 of ephrin B1 disrupts the ephrinB1/Dishevelled interaction, thus modulating retinal progenitor movement that is dependent on the planar cell polarity pathway.
The protein encoded by this gene is a type I membrane protein and a ligand of Eph-related receptor tyrosine kinases. It may play a role in cell adhesion and function in the development or maintenance of the nervous system.
, EPH-related receptor tyrosine kinase ligand 2
, ELK ligand
, CEK5 receptor ligand
, Cek ligand
, Cek5 ligand
, stimulated by retinoic acid gene 1 protein
, eph-related receptor tyrosine kinase ligand 2
, ligand of eph-related kinase 2
, ephrin-B1 (EPH family ligand)
, CEK5 ligand