EFNA5 (Ephrin A5)

The dualistic nature of Eph/ephrin signaling underscores its translational promise as both a biomarker framework and a precision-guided therapeutic target. Combinatorial receptor-ligand modulation strategies may advance the treatment of central nervous system malignancies by exploiting the context-dependent roles of Eph/ephrin interactions.

Moreover, the cis interaction interferes with ligand binding in trans , attenuates EphA2 canonical signaling. Our results uncover a new mechanism of EphA2 regulation by its co-expressed ligand ephrin-A1 with important implications in its known roles in oncogenesis as well as other disease processes including development of cataract.

This study presents a machine learning-based single-cell framework that systematically maps pancreatic cellular alterations in diabetes. The identified novel signatures, stellate activation dynamics, and beta cell maturation trajectories may serve as potential targets for diabetic management and pancreatic cancer risk stratification.

Small EVs derived from IFN-γ and TGF-β1-licensed MSCs exhibit demonstrate dose-dependent immunomodulatory trends in vitro, with enhanced effects observed at higher concentrations. These findings suggest their potential utility in modulating both innate and adaptive immune responses, warranting further investigation for their application as a cell-free therapeutic strategy in immune-mediated conditions.

We show that in hRMS ephrin-A5 binds and signals to EphA8 and EphA7 binds and signals to ephrin-A2, and that Fc chimeras of both molecules are potent inhibitors of hRMS proliferation. These results identify key differences between hRMS and normal muscle cells and support further research into Eph: ephrin signaling as potential differentiation therapies.

Furthermore, EFNA5 is an independent risk factor for poor prognosis in PAAD patients, and it can promote the malignant progression of pancreatic cancer in vitro and in vivo. Differential expression of EFNA1-5 is associated with TIME in pancreatic cancer, predicts different survival outcomes, and maybe a novel prognostic marker reflecting an immunosuppressive state and a potential therapeutic target.

XYP may treat TC by regulating SMIM1, PPP1R16A, KIAA1462, DNAJC22, EFNA5, and associated immune pathways; this provides theoretical support for its potential mechanisms.

These two derivatives inhibit ligand induced EphA4 activation in cells with sub-micromolar potency. Since they retain high potency and specificity for EphA4, lipidated and PEGylated APY-d3 derivatives represent new tools for discriminating EphA4 activities in vivo and for preclinical testing of EphA4 inhibition in animal disease models.

We hypothesize that canonical ligand-dependent EphA2 signaling is required for the morphogenesis and organization of hexagonal equatorial epithelial cells while non-canonical ligand-independent EphA2 signaling is needed for complex membrane interdigitations that change during fiber cell differentiation and maturation. This is the first demonstration of non-canonical EphA2 activation in a non-cancerous tissue or cell and suggests a possible physiological function for ligand-independent EphA2 signaling.

The expression of EFNA5 was low in hepatoma cells. An increase in EFNA5 levels hinders the proliferation, invasion, and migration of hepatoma cells. These effects may occur through inhibition of hepatoma epithelial-mesenchymal transition by EFNA5. Moreover, the study on the mechanisms of proliferation, invasion and metastasis of hepatoma provides a novel theoretical basis, and may influence the clinical practice of tumor treatment in the future.

The EphA-mediated signaling suppresses the ERK-ELK pathway, leading to the reduction of stomatin expression that affects prostate cancer malignancy.

CDD-2693 and CDD-3167 decreased expansion of primary endometrial epithelial organoids from patients with endometriosis and decreased Ewing's sarcoma viability. Thus, using DECL, we identified potent pan-EPH inhibitors that show specificity and activity in cellular models of endometriosis and cancer.