Date published: 2025-9-13

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V1RD4 Activators

Chemical activators of V1RD4 can initiate a cascade of intracellular events leading to the protein's activation. Forskolin, for instance, directly targets adenylyl cyclase, catalyzing the conversion of ATP to cyclic AMP (cAMP). The surge in cAMP levels results in the activation of protein kinase A (PKA), which can phosphorylate V1RD4, thereby activating it. Isoproterenol operates on a similar principle; as a beta-adrenergic agonist, it boosts intracellular cAMP levels, again promoting PKA activity that can lead to the phosphorylation and activation of V1RD4. Similarly, Prostaglandin E2 and Histamine, through their respective receptors, elevate cAMP levels, further contributing to PKA-mediated activation of V1RD4. Epinephrine also engages in this pathway, binding to beta-adrenergic receptors and escalating cAMP production, which subsequently activates PKA, and this kinase can phosphorylate and activate V1RD4. Glucagon follows the same route by binding to its specific receptor and increasing cAMP, which activates PKA that can then activate V1RD4 through phosphorylation.

In parallel, Vardenafil and Sodium Nitroprusside affect the cyclic guanosine monophosphate (cGMP) pathway. Vardenafil inhibits phosphodiesterase type 5, which usually breaks down cGMP. The resulting accumulation of cGMP leads to protein kinase G (PKG) activation. PKG can then activate V1RD4 through phosphorylation. Sodium Nitroprusside, by releasing nitric oxide, stimulates guanylyl cyclase to produce cGMP, which activates PKG that is capable of activating V1RD4. Furthermore, Angiotensin II and Diacylglycerol both activate protein kinase C (PKC) through different mechanisms - Angiotensin II via the AT1 receptor leading to phospholipase C (PLC) activation and Diacylglycerol acting directly. Once activated, PKC can phosphorylate and activate V1RD4. Anisomycin is yet another activator that employs the JNK signaling pathway, which includes kinases that phosphorylate and activate V1RD4. These chemical activators, each with their distinct mode of action, converge on the common outcome of activating V1RD4 through phosphorylation by different kinases.

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