Cell surface transmembrane ligand[4][6], Receptor ligand, Receptor (specifically binds to Eph receptors, which are receptor tyrosine kinases)[2][4], Other (classified within the ephrin family, structurally as a transmembrane protein, not a standalone enzyme or transporter)
01
Overview
Ephrin-B2 is a cell surface transmembrane ligand encoded by the EFNB2 gene. It belongs to the ephrin-B class and primarily interacts with Eph receptors, a family of receptor tyrosine kinases. Ephrin-B2 plays crucial roles in angiogenesis by regulating endothelial cell proliferation, migration, and vessel remodeling. It mediates bidirectional signal transduction—acting as both ligand and signaling molecule itself. In the context of disease, ephrin-B2 is associated with several processes including cancer progression, neural development, and cardiovascular homeostasis. Additionally, ephrin-B2 serves as a functional cell entry receptor for Hendra and Nipah viruses. Due to its central role in multiple essential biological pathways, ephrin-B2 is a recognized therapeutic target, but efforts to modulate its activity must carefully consider potential systemic effects and safety challenges[1][2][3][4][6].
Other names
EFNB2EFNB class ephrin[2][6]ephrinB2ephrin B2
02
Mechanism of action
Antagonism of Eph/ephrin interaction—blocking ligand-receptor binding and downstream signal transduction[3]; Inhibition of angiogenesis by disrupting Ephrin-B2/Eph receptor signaling[1]; Blocking viral entry (potential application for inhibitors in Hendra/Nipah viral infection)[2][3]
03
Biological functions
Angiogenesis (formation of new blood vessels)[1]Cell migration, motility, and adhesion[4][6]Signal transduction via bidirectional signaling (forward via Eph receptor, reverse via ephrin ligand)[2][1]Cellular morphology regulation[1]Developmental processes, including neural development and erythropoiesis[2]Immune response (through roles in tissue morphogenesis and cell-cell interactions in immune tissues)[5]
04
Disease associations
Cancer (upregulated in tumor neovascularization; downregulated in HPV-positive cervical neoplastic keratinocytes)[1][2]Cardiovascular disease (angiogenesis, vascular remodeling)[1]Neurodevelopmental disorders (roles in axon guidance and neural circuit formation)[3]Infection (acts as receptor for Hendra Virus and Nipah Virus, mediating pathogen entry)[2][3]Other (tissue injury and wound healing, via promoting neovascularization)[1]
05
Safety considerations
Ubiquitous and critical developmental/physiological roles elevate risk of off-target effects[1][2]Targeting ephrin-B2 or its pathway may induce vascular defects, impaired wound healing, and developmental abnormalitiesViral entry function raises caution for use in infection-related contexts[2][3]Potential for broad impacts on cell migration and tissue homeostasis
06
Interacting drugs
Small molecule antagonists targeting EphA4-ephrin-B2 interaction have been described in structural studies[3]
1 more in the full profile.
07
Biomarkers
Expression level in tumors as a prognostic marker for cervical neoplastic lesions progression[2]Upregulation at sites of neovascularization (tumors, wounds)[1]Potential biomarker for patient selection in angiogenesis-targeted therapies
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