Date published: 2025-9-11

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ephrin-2 Activators

Ephrin-2 is a pivotal protein in the family of ephrins, which are divided into two classes: the ephrin-As, which are anchored to the cell membrane by a glycosylphosphatidylinositol linkage, and the ephrin-Bs, which include ephrin-2 and are transmembrane proteins. Ephrin-2, also known as EFNB1, plays a crucial role in various developmental processes by interacting with Eph receptors, which are themselves part of a large family of receptor tyrosine kinases. These interactions are essential for cell signaling related to the establishment of tissue architecture during embryonic development and continue to participate in the regulation of cellular processes in adult tissue. The signaling cascade initiated by ephrin-2 binding can result in alterations in cellular shape, movement, and attachment, making it integral to processes such as neuronal mapping, angiogenesis, and bone remodeling. The expression of ephrin-2, therefore, is tightly controlled and can be influenced by various intracellular and extracellular cues that govern its role in physiological contexts.

Understanding the regulation of ephrin-2 is of significant interest in the field of molecular biology and biochemistry. Certain chemical compounds have the potential to induce the expression of ephrin-2, albeit through indirect pathways. For instance, retinoic acid may stimulate ephrin-2 expression by engaging nuclear receptors that bind to DNA response elements of the EFNB1 gene, initiating transcription. Similarly, Vitamin D3, through its hormonal form, could activate vitamin D response elements that increase ephrin-2 synthesis. Polyphenolic compounds like Epigallocatechin gallate (EGCG) might trigger a cascade of signaling events leading to the activation of transcription factors that promote EFNB1 gene expression. Furthermore, small molecule inhibitors such as sodium butyrate act epigenetically, modifying the chromatin structure around the EFNB1 gene, thereby facilitating transcription. Each of these compounds, from natural derivatives like curcumin, which may inhibit pathways suppressing EFNB1, to synthetic molecules like dexamethasone, which may bind to specific elements within the gene's promoter region, exemplifies the diverse mechanisms by which ephrin-2 expression could potentially be upregulated. The study of these activators provides insight into the intricate regulatory networks that maintain cellular function and homeostasis.

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