Final answer:
The GPCR pathway is turned off when the active G-protein hydrolyzes GTP to GDP, causing the alpha and beta-gamma subunits to reassociate into an inactive state. Certain hormones like somatostatin can decrease cAMP levels, aiding in the deactivation process. Proper termination of signaling is crucial for cellular function and to prevent diseases.
Step-by-step explanation:
The GPCR pathway is shut off through a series of regulatory mechanisms. The active G-protein, which was activated when a signaling molecule such as a hormone binds to the G-protein-coupled receptor, eventually hydrolyzes the bound GTP to GDP. After the hydrolysis of GTP, the G protein subunits, specifically the alpha (α) subunit and the beta-gamma (βγ) complex, reassociate to form the inactive G-protein, readying the system for another cycle. In some cases, such as the action of somatostatin, the level of secondary messenger cAMP is decreased, further contributing to the deactivation of the pathway and inhibiting responses such as the secretion of human growth hormone.
Additionally, the termination of the cell signaling cascade is important to maintain proper cellular function. Signaling molecules are degraded and signaling intermediates are dephosphorylated to ensure the cellular response is appropriate in timing and intensity. Conditions where these pathways are blocked or defective can lead to diseases, showing the critical nature of these regulatory mechanisms.