Q.29 The receptor for epinephrine is a
(A) Tyrosine kinase receptor (B) Serine–threonine kinase receptor
(C) G–protein–coupled receptor (D) Ligand activated transcription factor
Answer: (C) G-protein-coupled receptor
Epinephrine (adrenaline) binds to adrenergic receptors (α and β subtypes), which are classic G-protein-coupled receptors (GPCRs) featuring seven transmembrane domains. These receptors activate G-proteins to modulate second messengers like cAMP (β receptors) or IP3/Ca²⁺ (α1), distinguishing them from kinase-linked or nuclear receptors.
Option Analysis
(A) Tyrosine kinase receptor: Incorrect—RTKs (e.g., insulin receptor) autophosphorylate tyrosines upon ligand binding; epinephrine receptors lack this intrinsic kinase activity.
(B) Serine-threonine kinase receptor: Incorrect—STKs (e.g., TGF-β receptors) phosphorylate Ser/Thr residues; adrenergic signaling uses G-protein cascades, not direct kinase domains.
(C) G-protein-coupled receptor: Correct—all adrenergic receptors (α1, α2, β1-3) belong to the GPCR superfamily, coupling to Gs, Gi, or Gq proteins.
(D) Ligand activated transcription factor: Incorrect—nuclear receptors (e.g., steroid hormones) directly bind DNA; epinephrine acts via membrane GPCRs for rapid signaling.
Introduction: Epinephrine Receptor G-Protein-Coupled Receptor
The epinephrine receptor classification as a G-protein-coupled receptor (GPCR) is fundamental in biochemistry and pharmacology. This article analyzes why adrenergic receptors are GPCRs, not tyrosine kinase or serine-threonine kinase receptors, with exam-focused option explanations.
Receptor Classification Table
| Receptor Type | Examples | Mechanism | Epinephrine? |
|---|---|---|---|
| Tyrosine Kinase (RTK) | Insulin, EGFR | Dimerization → Tyr phosphorylation | No |
| Ser/Thr Kinase | TGF-β, BMP receptors | Heterodimer → Ser/Thr signaling | No |
| GPCR (7TM) | Adrenergic α/β | G-protein → cAMP/Ca²⁺ | Yes |
| Nuclear Receptor | Glucocorticoid | DNA binding → transcription | No |
Signaling Pathways
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β-receptors: Gs → adenylyl cyclase → ↑cAMP → PKA activation (heart stimulation).
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α1-receptors: Gq → PLC → IP3/DAG → Ca²⁺ release (vasoconstriction).
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α2-receptors: Gi → ↓cAMP (presynaptic inhibition).
This GPCR mechanism enables epinephrine’s rapid “fight-or-flight” responses, contrasting slower transcriptional regulation. Critical for molecular biology and biochemical engineering curricula.
