Final answer:
The G-protein/cAMP/CREB pathway involves a hormone activating a G-protein-coupled receptor, which then activates adenylyl cyclase leading to the production of cAMP. cAMP activates PKA, which can phosphorylate the transcription factor CREB, influencing gene expression. This pathway exemplifies signal amplification and is tightly regulated to ensure appropriate cellular responses.
Step-by-step explanation:
The G-protein/cAMP/CREB pathway is a crucial signaling mechanism in cells, whereby extracellular signals are transmitted into the cell to elicit a response. The pathway begins when a hormone like epinephrine binds to a G-protein-linked receptor on the cell surface. This binding leads to a conformational change that allows GTP to replace GDP on the G-protein, activating it. The activated G-protein then interacts with and activates adenylyl cyclase, an enzyme that converts ATP into the second messenger cAMP (cyclic Adenosine Monophosphate).
Once formed, cAMP activates protein kinase A (PKA), which phosphorylates various substrates resulting in changes to their activity. One such substrate can be the transcription factor CREB (cAMP response element-binding protein), which, when phosphorylated by PKA, can modulate gene expression. This cascade effect demonstrates how a single extracellular signal can result in a significant intracellular response, known as signal amplification, affecting various cellular processes including glycogen breakdown among others. To terminate the signal, cAMP is broken down by phosphodiesterase, thereby stopping further activation of PKA and the downstream effects.