cAMP as a second messenger — primary intracellular effect Which statement correctly describes a key intracellular action when cyclic AMP (cAMP) functions as a second messenger?

Introduction / Context:
cAMP is a ubiquitous second messenger produced by adenylyl cyclase downstream of many G-protein–coupled receptors. Its central task is to translate receptor activation into changes in enzyme activities and gene expression via protein phosphorylation pathways.

Given Data / Assumptions:

• Hormones/ligands (first messengers) are extracellular; cAMP is intracellular.
• cAMP binds regulatory subunits of PKA to release active catalytic subunits.
• Tissue-specific responses arise from distinct PKA targets and scaffolding (AKAPs).

Concept / Approach:

The canonical pathway is GPCR → Gαs → adenylyl cyclase → cAMP ↑ → PKA activation. Activated PKA phosphorylates metabolic enzymes, ion channels, and transcription factors (e.g., CREB), producing coordinated physiological effects such as glycogen breakdown or increased heart rate.

Step-by-Step Solution:

Verification / Alternative check:

Pharmacological agents that raise cAMP levels (e.g., forskolin, PDE inhibitors) mirror PKA-mediated effects, confirming this mechanism.

Why Other Options Are Wrong:

Option A trivializes cAMP and misstates its relation to AMP. Option B is false; cAMP specifically activates PKA (and certain cyclic nucleotide–gated channels), not all kinases. Option D confuses first and second messengers. Option E overgeneralizes channel regulation.

Common Pitfalls:

Assuming cAMP equals “active everything.” Signaling specificity depends on compartmentalization and defined targets.

Final Answer:

It activates the cAMP-dependent protein kinase (PKA)