Anti-EFNA1 / Ephrin A1

In 1X PBS, pH 7.4, with 0.09% sodium azide and 50% glycerol. Ephrin A1 is a membrane-bound protein that interacts with Eph receptors on neighboring cells, initiating a cascade of signals that regulate cell behavior and movement. This interaction is essential for processes such as cell migration, tissue organization, and synaptic connectivity in the nervous system. Studies have shown that dysregulation of Ephrin A1 signaling can lead to aberrant cell growth, invasion, and metastasis in cancer cells, highlighting its importance in disease progression. One of the key features of Ephrin A1 is its ability to both attract and repel cells, depending on the context and concentration of the molecule. This dual role allows Ephrin A1 to fine-tune cell-cell interactions and ensure proper tissue patterning during development. In the brain, for example, Ephrin A1 guides axonal growth and synapse formation, shaping the intricate neural circuits that underlie cognitive functions. In addition to its role in development, Ephrin A1 has also been implicated in several disease processes. Aberrant expression of EFNA1 has been observed in various types of cancer, including breast, lung, and colon cancer, where it promotes tumor growth and invasion. In neurodegenerative disorders such as Alzheimer's disease, dysregulation of Ephrin A1 signaling disrupts synaptic connectivity and contributes to cognitive decline. Protein function: Cell surface GPI-bound ligand for Eph receptors, a family of receptor tyrosine kinases which are crucial for migration, repulsion and adhesion during neuronal, vascular and epithelial development. Binds promiscuously Eph receptors residing on adjacent cells, leading to contact-dependent bidirectional signaling into neighboring cells. Plays an important role in angiogenesis and tumor neovascularization. The recruitment of VAV2, VAV3 and PI3-kinase p85 subunit by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly. Exerts anti-oncogenic effects in tumor cells through activation and down- regulation of EPHA2. Activates EPHA2 by inducing tyrosine phosphorylation which leads to its internalization and degradation. Acts as a negative regulator in the tumorigenesis of gliomas by down- regulating EPHA2 and FAK. Can evoke collapse of embryonic neuronal growth cone and regulates dendritic spine morphogenesis. [The UniProt Consortium]