1. What are the terms found in the Michaelis-Menten equation and what do they mean? Draw a graph of vi versus [S] for a hypothetical Machaelis-Menten enzyme. What kind of curve is derived? Where are Vmax and KM on this curve?
2. Are glucokinase and hexokinase isozymes? Is hexokinase a Michaelis-Menten enzyme? Is glucokinase of liver or pancreas a Michaelis-Menten enzyme?
3. How does the S0.5 for pancreatic glucokinase in some patients with MODY compare with normal patients? What effect does this have on insulin production and blood glucose levels?
4. What is the effect of a competitive inhibitor on the KM and Vmax?
5. What is the effect of a noncompetitive inhibitor on the KM and Vmax?
6. How does product inhibition of hexokinase in one cell benefit all the other cells of the body?
7. What are the various names for the compounds that bind to an allosteric site? What affect do they have on the enzyme?
8. The substrates of allosteric enzymes exhibit positive cooperativity. Explain positive cooperativity in terms of subunits, conformation, and activity of the active site.
9. What is the difference between the T-conformation (state) and the R-conformation of an allosteric enzyme?
10. Understand the effect that allosteric activators and inhibitors have on the conformation of an allosteric enzyme and on the plot of velocity versus substrate concentration. What about the S0.5?
11. What is the general name for the enzyme that places phosphate groups onto an.enzymes? What groups on the enzymes are typically phosphorylated? What are the effects of phosphorylation?
12. What is the general name for the enzymes that hydrolyze and thus remove phosphate groups from proteins? What bond is usually broken? What are the effects of dephosphorylation?

13. Using the terms seryl residue, phosphorylation, positive allosteric effector allosteric site, phosphorylase b, phosphorylase a, conformation, and enzyme activity, explain how either AMP or phosphorylase kinase activates muscle glycogen phosphorylase. What is the effect of protein phosphatase upon phosphorylase a?
14. What are the activators of phosphorylase kinase in a muscle cell?
15. Starting with an increase in the concentration of cAMP that resulted from adrenalin binding to a receptor in the cell membrane, explain how phosphorylase is activated. How does the cascade result in the amplification of the original signal?

16. Explain how an increase in calcium in muscle cells simultaneously activates muscle contraction and glycogenolysis. Which system uses ATP and which helps to produce ATP?
17. How do G-proteins function? No need to mention GAPs, GEFs, GDIs, or the Ras family at this time.
18. Are chymotrypsinogen and prothrombin zymogens? How are these enzymes activated?
19. What is the time frame of induction or repression?
20. Name one hormone that induces ubiquitin in muscle tissue. What is the function of this process, i.e., what is the result of ubiquitin induction?
21. Why is it important that the regulatory (control) enzyme for a pathway, catalyze the rate limiting step in a pathway? How is the rate of this step (enzyme) controlled? What does the term committed step mean?
22. Concerning Al Martini, what are the two principal mechanisms for catabolizing ethanol in humans? Be able to write the reaction for the most common mechanism that uses NAD+ as a cofactor.
23. Concerning Al Martini, assume that the Vmax of cytosolic alcohol dehydrogenase enzyme and the MEOS system are equal in Al's liver and that the KM's are 0.04 mM and 11 mM, respectively. Which will oxidize most of the alcohol consumed when the blood alcohol content is low. For example, after consuming 1 oz of alcohol and a blood alcohol of 6.4 mM. Why?
24. Concerning Al Martini, explain how increasing the amount of alcohol oxidized by alcohol dehydrogenase will affect the rate at which alcohol is oxidized. How does this affect fatty acid oxidation?
25. Concerning Ann O'Rexia, in which of her tissues do you find hexokinase and glucokinase and what is the reaction these enzymes catalyze? When glucose-6-phosphate inhibits hexokinase, is this product inhibition?
26. Concerning Ann O'Rexia, what pathway is used when her cells wants to make energy from glucose-6-phosphate and how does the concentration of ATP or AMP in the cell affect the rate of this pathway? Is ATP a feedback inhibitor? Is ATP a negative allosteric effector and/or allosteric inhibitor? Is AMP a positive allosteric effector and/or allosteric activator?

27. Concerning Ann O'Rexia, what pathway does she use for the storage of glucose as glycogen? How does glucose concentration and insulin affect this pathway?

28. Concerning Ann O'Rexia who suffers from anorexia, if joging activates both glycogenolysis and glycolysis, why does Ann tire easily?
29. Concerning Ann O'Rexia, when she begins to jog, what muscle enzyme in glycogenolysis is activated by AMP? What type of activation is this? How does epinephrine activate this same enzyme? What role does cAMP and protein kinase A play in this cascade?
30. Concerning Ann O'Rexia, when she begins to jog, what enzyme in glycolysis is activated? What type of activation is this?


Adrenaline, allosteric activator, allosteric effector, allosteric enzyme, allosteric inhibitor, amplified, cAMP, calmodulin, epinephrine, feedback inhibition, glucokinase, glucose, glucose 6-phosphate, glycogen phosphorylase, hexokinase, initial velocity, isozyme, K0.5, Km, modulator proteins, phosphoester, phosphorylation cascade, positive allosteric effector, product inhibition, protein kinase, protein kinase A, protein phosphatase, proteolytic cleavage, R- state, rectangular hyperbola, velocity, S0.5, serine/threonine kinase, substrate, T- conformation, troponin-C, tyrosine kinase, Vmax, zymogen


Understand the meaning of the key words in the context of Chapter 9.

Examine Questions (Q:)and Answers(A:) in Chapter 9.

Work Review Questions 1, 3, and 5 but not 2 and 4 at the end of the Chapter 9.

Work the Practice Questions for Chapter 9 Objectives

Other Help:

Competitive and Noncompetitive Enzyme Inhibition Graph

cAMP Cascade