OR7G1 Activators

OR7G1 can elicit their effects through various intracellular signaling pathways. Acetylcholine, for instance, engages with muscarinic and nicotinic receptors, initiating a cascade of G-protein coupled reactions that can lead to OR7G1 activation. Similarly, sodium fluoride serves as a G-protein activator, thus enhancing the production of cAMP by adenylyl cyclase, which subsequently activates protein kinase A (PKA). PKA is then able to phosphorylate target proteins, which may include OR7G1, changing its activity state. Forskolin also raises intracellular cAMP concentrations directly by stimulating adenylyl cyclase, which then triggers PKA, leading to the phosphorylation of OR7G1. Ionomycin, by increasing intracellular calcium levels, could activate calcium-dependent kinases that may then target proteins involved in olfactory signaling, including OR7G1.

Isoproterenol targets beta-adrenergic receptors, resulting in elevated cAMP levels and PKA activation, which can phosphorylate OR7G1. Histamine connects with its receptors to influence signaling pathways involving cAMP and PKA, possibly affecting OR7G1 activity. Adenosine, specifically through the A2 receptor subtype, can increase cAMP production, leading to PKA-mediated phosphorylation of OR7G1. Pilocarpine, acting on muscarinic acetylcholine receptors, engages G-protein coupled pathways that could result in OR7G1 activation. Capsaicin activates TRPV1, leading to calcium influx and activation of calcium-dependent signaling pathways, which could culminate in the activation of OR7G1. Nicotine binds to nicotinic acetylcholine receptors, which modulates neuronal signaling pathways that could affect OR7G1. Olfactomedin 2, as an extracellular matrix glycoprotein, modulates olfactory receptor neuron responsiveness, potentially affecting OR7G1 activation. Lastly, zinc gluconate provides zinc ions, which can modulate receptor activity and influence the activity state of OR7G1.