Forskolin directly activate adenylyl cyclase resulting in increased intracellular cAMP. This elevation in cAMP can promote the signaling of GPCRs, including OR1N2, by enhancing the activity of protein kinase A (PKA) and the subsequent phosphorylation cascade that modulates GPCR function. Inhibitors of phosphodiesterase such as IBMX, caffeine, and theophylline serve to sustain heightened levels of cAMP by preventing its breakdown, thereby extending and intensifying the activation of GPCRs akin to OR1N2. PGE2 and histamine, through their respective receptors, can also regulate cAMP concentrations, which in turn can alter OR1N2 activity.
Nicotine has the capacity to influence the family of GPCRs by its interaction with nicotinic acetylcholine receptors, which can lead to diverse intracellular events affecting GPCR function. Capsaicin and menthol, known for their effects on TRP channels, can influence intracellular calcium levels, a secondary messenger that plays a critical role in GPCR signaling. L-Arginine is involved in the production of nitric oxide, which can influence GPCR signaling through cGMP-dependent pathways, potentially impacting OR1N2. Sodium butyrate can lead to changes in the expression of GPCRs, influencing the signaling of receptors like OR1N2. Guanosine 5'-O-(3-thiotriphosphate) tetralithium salt is a non-hydrolyzable GTP analog that can activate G proteins, which are essential in GPCR signaling, thereby potentially enhancing the activity of OR1N2.
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