cAMP exerts its intracellular effects primarily by activating which protein?

Explanation

## cAMP and Protein Kinase A **Key Point:** cAMP is a second messenger that activates Protein Kinase A (PKA), also called cAMP-dependent protein kinase. PKA then phosphorylates downstream target proteins to produce cellular responses. ### cAMP Signaling Cascade 1. Extracellular hormone (e.g., epinephrine, glucagon) binds Gs-coupled GPCR 2. Gs activates adenylyl cyclase → ↑ cAMP 3. cAMP binds regulatory (R) subunits of PKA, releasing catalytic (C) subunits 4. Active PKA phosphorylates target proteins (glycogen phosphorylase kinase, CREB, etc.) 5. Cellular response: glycogenolysis, lipolysis, increased heart rate ### cAMP vs. IP₃/DAG Pathways | Feature | cAMP Pathway | IP₃/DAG Pathway | |---|---|---| | Activating enzyme | Adenylyl cyclase | Phospholipase C | | Second messenger | cAMP | IP₃ + DAG | | **Primary effector** | **Protein Kinase A** | **IP₃ receptor (Ca²⁺ release) + Protein Kinase C** | | Typical hormone | Epinephrine, glucagon | Angiotensin II, vasopressin | **High-Yield:** PKA is the **only** major effector of cAMP in mammalian cells. This is a direct, high-frequency NEET PG recall item. **Mnemonic:** **cAMP → PKA → Phosphorylation** — remember the three P's. **Clinical Pearl:** β-blockers inhibit epinephrine signaling by blocking the GPCR, thereby reducing cAMP and PKA activation—explaining their use in hypertension and angina.