Table of contents

1. Introduction to Biochemistry4h 34m
2. Water3h 23m
3. Amino Acids8h 10m
4. Protein Structure10h 4m
5. Protein Techniques14h 5m
6. Enzymes and Enzyme Kinetics13h 38m
7. Enzyme Inhibition and Regulation 8h 42m
8. Protein Function 9h 41m
9. Carbohydrates7h 49m
10. Lipids5h 49m
11. Biological Membranes and Transport 6h 37m
12. Biosignaling9h 45m
Review 1: Nucleic Acids, Lipids, & Membranes2h 47m
Review 2: Biosignaling, Glycolysis, Gluconeogenesis, & PP-Pathway3h 12m
Review 3: Pyruvate & Fatty Acid Oxidation, Citric Acid Cycle, & Glycogen Metabolism2h 26m
Review 4: Amino Acid Oxidation, Oxidative Phosphorylation, & Photophosphorylation1h 48m

12. Biosignaling

Drugs & Toxins Affecting GPCR Signaling

Biochemistry

12. Biosignaling

Drugs & Toxins Affecting GPCR Signaling

Previous problemNext problem

Struggling with Biochemistry?

Join thousands of students who trust us to help them ace their exams!Watch the first video

Multiple Choice

Pertussis toxin is produced by Bordetella pertussis, the bacterium that causes whooping cough. Pertussis toxin catalyzes the addition of ADP-ribose to G_i which 'locks' it in the GDP-bound state. If the uninhibited, toxin free GPCR pathway normally results in decreased glycogen synthesis, then what would be the effect of pertussis toxin?

It would decrease contraction.

It would decrease glucose production.

It would further decrease glycogen production.

It would increase the rate of endocytosis.

Previous problemNext problem

Verified step by step guidance

Understand the role of Gi protein in the GPCR pathway: Gi is an inhibitory G protein that, when activated, inhibits adenylate cyclase, leading to decreased levels of cAMP. This results in reduced activation of protein kinase A (PKA), which in turn decreases glycogen breakdown and increases glycogen synthesis.

Recognize the effect of pertussis toxin: Pertussis toxin ADP-ribosylates the Gi protein, locking it in its inactive GDP-bound state. This prevents Gi from inhibiting adenylate cyclase, leading to increased cAMP levels.

Analyze the impact on glycogen synthesis: With increased cAMP levels due to the inactivation of Gi, PKA remains active. Active PKA promotes glycogen breakdown and inhibits glycogen synthesis.

Connect the pathway changes to the problem statement: The uninhibited GPCR pathway normally decreases glycogen synthesis. However, with pertussis toxin locking Gi in the inactive state, the pathway is further shifted towards glycogen breakdown.

Conclude the effect of pertussis toxin: Since the pathway is shifted towards increased glycogen breakdown, the effect of pertussis toxin would be to further decrease glycogen production, aligning with the correct answer provided.