Date published: 2025-11-1

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E130203B14Rik Activators

Vstm4, a V-set and transmembrane domain-containing protein, intricately governs processes like endothelial cell migration, retina blood vessel maintenance, and vasculature development. Positioned in the extracellular region and plasma membrane, Vstm4's orthologous human counterpart suggests conserved functional significance. To activate Vstm4, a diverse set of chemicals emerges. Retinoic Acid, by engaging RAR/RXR receptors, enhances endothelial cell migration and vasculature development via Vstm4 up-regulation. Forskolin elevates cAMP levels, indirectly activating Vstm4 and contributing to its regulatory role in endothelial cell migration and retina blood vessel maintenance.

Epigallocatechin Gallate acts by modulating MAPK signaling, linking Vstm4 to enhanced endothelial cell migration. Lithium Chloride triggers Vstm4 through Wnt/β-catenin, illustrating a connection between this pathway and Vstm4 activation. Nicotinamide indirectly activates Vstm4 by influencing SIRT1, connecting cellular metabolism to Vstm4 regulation. SB431542 inhibits TGF-β/Smad, creating a permissive environment for Vstm4 up-regulation. 2-Deoxy-D-glucose alters metabolism, impacting Vstm4 expression indirectly. Prostaglandin E1 stimulates Vstm4 through the cAMP/PKA pathway, providing an indirect mechanism for Vstm4 activation. Wortmannin inhibits PI3K/Akt, impacting Vstm4 indirectly. Niclosamide, by destabilizing β-catenin, connects Wnt signaling to Vstm4 activation. Trichostatin A modulates HDAC, offering an epigenetic avenue for Vstm4 up-regulation. JNK Inhibitor VIII suppresses JNK signaling, indirectly activating Vstm4. These chemicals unveil the intricate web of pathways influencing Vstm4, providing valuable insights into potential regulatory mechanisms governing its function in crucial cellular processes.

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JNK Inhibitor VIII

894804-07-0sc-202673
5 mg
$267.00
2
(1)

JNK Inhibitor VIII activates Vstm4 by inhibiting the JNK pathway. Suppression of JNK signaling enhances endothelial cell migration and vasculature development, indirectly influencing Vstm4 expression. The compound provides a pathway-specific mechanism for JNK-dependent Vstm4 up-regulation.