A researcher studies cells treated with pertussis toxin. Which cellular response will be lost?
- A Somatostatin-mediated inhibition of cAMP production via Gi-coupled SSTR ✓
- B Glucagon-stimulated cAMP rise via Gs-coupled glucagon receptor
- C IP3 generation from PLC-beta activation by Gq-coupled receptors
- D Insulin-receptor-mediated tyrosine kinase phosphorylation of IRS-1
Explanation
Pertussis toxin ADP-ribosylates and permanently activates Gi-alpha, locking it in a form that cannot inhibit adenylyl cyclase. Consequently, Gi-coupled receptor signals (e.g., somatostatin via SSTR, alpha-2 adrenergic, adenosine A1) lose their ability to suppress cAMP. Gs-coupled signaling (glucagon) uses a different G-protein not affected by pertussis toxin. Gq-PLC-IP3 signaling and insulin receptor tyrosine kinase are independent of Gi.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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