8. In considering PDC regulation, why are reactants typically activators, and why are products typically inhibitors? What does phosphorylation (in mammals) do to this complex?
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- 6)During the epinephrine signaling pathway we learned about in class, the enzyme glycogen phosphorylase is regulated by: Zymogen activation Competitive inhibition Allosteric regulation Covalent modification4. Hexokinase is kinase that catalyzes the phosphorylation of glucose by ATP to glucose-6-P, which can bind toits active site, blocking the access to ATP. Which of the following statements is/are correct regarding the typeof regulation?a) Phosphorylationb) Dephosphorylation.c) Feedback inhibition.d) Repression Explain each of the following optionDescribe the possible roles of allosteric modulation in theregulation of metabolic pathways.
- 3. It is known that Leber hereditary optic neuropathy (LHON) is an inherited form of blindness due to the missense mutations of mitochondrially encoded proteins of complexes I or III of the ETC. Explain why disorder in the structure of these components of ETC can impair clectron transport and oxidative phosphorylation. For the answer: a) draw the scheme of ETC and describe the structure of its components; b) explain how the electrochemical gradient is generated during the transport of the electrons; c) explaine what the respiratory control of the ETC and P/O ratio is.5. Gout can be caused by superactivation of PRPP synthase, or partial deficiency of hypoxanthine-guanine phosphoribosyl transferase. Why the change in these enzyme activities can induce the development of this disorder? For the answer: a) write down the scheme of the reactions catalyzed by these enzymes;b) specify metabolic pathways these reactions take part in; c) answer the main question of the problem.A 65-year-old man with severe atherosclerotic coronary artery disease comes to the emergency department because of a 12-hour history of chest pain. Plasma activity of the MB isozyme of creatine kinase (MB-CK) is markedly increased. Which of the following processes is the most likely explanation for the increased plasma MB-CK? (A) Cell membrane damage (B) Endoplasmic reticulum dilation (C) Mitochondrial swelling (D) Polysome dissociation (E) Sodium pump dysfunction
- 9. In a patient with a hereditary disease caused by liver phosphorylase kinase defect, hepatomegaly is observed (an increase in liver size), glycogen of the normal structure accumulates in the liver cells, moderate hypoglycemia is observed 3 hours after a meal. Explain the listed symptoms and the accumulation of unchanged structure glycogen in this pathology. For this: a) draw a process diagram in which phosphorylase kinase is involved; b) indicate the metabolic block on the diagram and explain the symptoms observed in the patient.5. Based on your understanding of allosteric regulation and using terminology related to the allosteric (MWC) model, explain how the enzyme glycogen phosphorylase is affected by the binding of AMP and what affect this binding would have on the overall activity of the enzyme. Predict what would happen to the activity of the enzyme when glycogen phosphorylase is covalently modified and there are high levels of ATP in the cell.Identify the type of regulation of enzyme activity seen in the following situations - for example, competitive inhibition, allosterism, phosphorylation, zymogen conversion, association-dissociation, feedback inhibition, etc. a. Trypinsogen, which is not catalytically active, is converted to the active enzyme trypsin by removal of a hexapeptide from the N-terminal end. b. The dimer protein kinases is catalytically inactive. Binding of cAMP causes protein kinase dimer to split into its monomer which are active catalysts.
- How would chymotrypsin's catalytic triad be affected by extremely low and extremely high pH values (assuming the rest of the protein remains intact)?1. Consider the enzyme pyruvate carboxylase. a. What pathway(s) does this enzyme function in? b. What cofactor does this enzyme use? c. Why is this cofactor required? d. How is this enzyme regulated? e. How does regulation of this enzyme impact the pathway(s) it operates in? How does regulation of this enzyme impact other pathway(s) we have discussed?4. (a) courses (such as this one) that NADH produced through glycoly- °H °H! sis in the cytosol can be used to generate ATP in the mitochon- dria. Yet, if 7-(14C)-NADH (in which the nicotinamide C-7 position is radioactively labeled; see diagram on the right) is added to rat hepatocytes, no radioactivity appears in the mitochondrial matrix while, if 4-(H)-NADH is added to hepatocytes, the tritium label soon appears in the mitochondrial matrix. Explain. It is generally stated and taught in biochemistry H H `NH2 NH2 R R [4-°H]NADH [7-14C]NADH