Vmn1r34, a vomeronasal type 1 receptor, emerges as a crucial player in the complex orchestra of chemosensory signaling, particularly within the context of pheromone detection and transduction. Positioned predominantly in the vomeronasal organ, Vmn1r34 acts as a molecular sentinel, deciphering chemical cues that govern social and reproductive behaviors across various species. The primary function of Vmn1r34 is intricately entwined with its role as a G protein-coupled receptor (GPCR). As an integral component of the chemosensory system, Vmn1r34 detects and responds to specific chemical stimuli, initiating a cascade of intracellular events that culminate in the activation of downstream signaling pathways.
The activation of Vmn1r34 hinges on a sophisticated interplay of molecular events, where chemical stimuli serve as keys to unlock the receptor's functional responses. The direct activators outlined in the table, such as forskolin and isoproterenol, exemplify the diverse mechanisms involved in Vmn1r34 activation. Forskolin, a diterpene, directly activates Vmn1r34 by stimulating adenylyl cyclase, leading to elevated cAMP levels. In parallel, isoproterenol, a beta-adrenergic agonist, engages with the receptor and initiates GPCR signaling, resulting in increased cAMP production. These signaling cascades converge on the activation of downstream protein kinase A (PKA), triggering a series of cellular responses associated with Vmn1r34. Moreover, the indirect activators, such as PGE2 and IBMX, showcase the complexity of activation by modulating the GPCR signaling pathway. Prostaglandin E2 (PGE2) binds to the receptor, initiating GPCR signaling, while IBMX prevents cAMP degradation, enhancing GPCR signaling. Both mechanisms contribute to the amplification of cellular responses mediated by Vmn1r34. Collectively, these insights into the molecular intricacies of Vmn1r34 activation underscore its pivotal role in orchestrating chemosensory responses, providing a foundation for further exploration of the complex mechanisms governing this GPCR's function in the context of pheromone signaling.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Isoproterenol Hydrochloride | 51-30-9 | sc-202188 sc-202188A | 100 mg 500 mg | $27.00 $37.00 | 5 | |
Isoproterenol, a beta-adrenergic agonist, directly activates Vmn1r34 by binding to its receptor, initiating GPCR signaling. This leads to increased cAMP production, activating downstream PKA and, consequently, the activation of Vmn1r34 and related cellular responses. | ||||||
8-Bromo-cAMP | 76939-46-3 | sc-201564 sc-201564A | 10 mg 50 mg | $97.00 $224.00 | 30 | |
8-Bromo-cAMP, a cAMP analog, directly activates Vmn1r34 by mimicking the intracellular signaling molecule. This artificial activator enhances GPCR signaling, leading to increased PKA activity and, ultimately, the activation of Vmn1r34 and associated cellular responses. | ||||||
8-CPT-cAMP | 93882-12-3 | sc-201569 sc-201569A | 20 mg 100 mg | $85.00 $310.00 | 19 | |
8-CPT-cAMP, a cAMP analog, directly activates Vmn1r34 by mimicking the intracellular signaling molecule. This artificial activator enhances GPCR signaling, leading to increased PKA activity and, ultimately, the activation of Vmn1r34 and associated cellular responses. | ||||||
PGE2 | 363-24-6 | sc-201225 sc-201225C sc-201225A sc-201225B | 1 mg 5 mg 10 mg 50 mg | $56.00 $156.00 $270.00 $665.00 | 37 | |
Prostaglandin E2 (PGE2), a signaling molecule, indirectly activates Vmn1r34 by binding to its receptor and activating GPCR signaling. This leads to enhanced cAMP levels, triggering downstream PKA activity, resulting in the activation of Vmn1r34 and related cellular responses. | ||||||
Propranolol | 525-66-6 | sc-507425 | 100 mg | $180.00 | ||
Propranolol, a non-selective beta-blocker, indirectly influences Vmn1r34 by blocking beta-adrenergic receptors. This inhibits GPCR signaling, reducing cAMP levels and suppressing downstream PKA activity, ultimately influencing the cellular responses associated with Vmn1r34. | ||||||
IBMX | 28822-58-4 | sc-201188 sc-201188B sc-201188A | 200 mg 500 mg 1 g | $159.00 $315.00 $598.00 | 34 | |
IBMX, a phosphodiesterase inhibitor, indirectly activates Vmn1r34 by preventing cAMP degradation. Elevated cAMP levels enhance GPCR signaling, leading to increased PKA activity and, consequently, the activation of Vmn1r34 and associated cellular responses. | ||||||
SQ 22536 | 17318-31-9 | sc-201572 sc-201572A | 5 mg 25 mg | $93.00 $356.00 | 13 | |
SQ22536, an adenylyl cyclase inhibitor, inhibits cAMP production, thereby indirectly influencing Vmn1r34 activation. By modulating the GPCR signaling pathway, it hinders downstream PKA activity, affecting the overall cellular responses associated with Vmn1r34. | ||||||
Adenosine 3′,5′-cyclic Monophosphate, N6-Benzoyl-, Sodium Salt | 30275-80-0 | sc-300167 | 10 µmol | $318.00 | 1 | |
6-Bnz-cAMP, a cAMP analog, directly activates Vmn1r34 by mimicking the intracellular signaling molecule. This artificial activator enhances GPCR signaling, leading to increased PKA activity and, ultimately, the activation of Vmn1r34 and associated cellular responses. | ||||||