1. The key regulatory enzyme of cholesterol synthesis is
A. HMG CoA synthase
B. HMG CoA lyase
C. HMG CoA reductase
D. Mevalonate kinase
1. The key regulatory enzyme of cholesterol synthesis is A. HMG CoA synthase B. HMG CoA...
QUESTION 4 The rate limiting enzyme for cholesterol synthesis is A Acyl-CoA-cholesterol acyl transferase (ACAT) B. HMG-CoA Lyase C. HMG-CoA Reductase D. HMG-CoA Synthase
HMG-CoA reducatse is the key regulatory enzyme in the biosynthesis of cholesterol. Outline briefly the various regulatory mechanisms involving HMG-CoA reductase in cholesterol biosynthesis.
HMG-CoA reductase, a critical enzyme in cholesterol synthesis is the target or statin inhibitors. You are characterizing a possible new inhibitor and want to determine its mode of binding to HMG-CoA reductase. Equilibrium dialysis measurements at 25°C, 30°C, and 37°C yielded dissociation constants (Ks) of 2.5 x 10* M, 1.5 x 10*, and 1.0 x 10* M, respectively, for the HMG- CoA reductase-inhibitor complex a. Is the binding becoming better or worse with increasing temperature? Explain. b. Using Excel or...
HMG-CoA reductase, a critical enzyme in cholesterol synthesis is the target or statin inhibitors. You are characterizing a possible new inhibitor and want to determine its mode of binding to HMG-CoA reductase. Equilibrium dialysis measurements at 25 C, 30°C, and 37 C yielded dissociation constants (K.) of 2.5 x 10" М, 1.5 x 10", and 1.0 x 103 M, respectively, for the HMG-CoA reductase-inhibitor complex. a. Is the binding becoming better or worse with increasing temperature? Explain. b. Using Excel...
Rachel is studying cholesterol synthesis in mice. Some mice had a mutation in their sterol regulatory element binding protein (SREBP) that is normally active when cholesterol levels are low in the cell. This mutation can no longer bind to the gene promoter for cholesterol synthesis pathway enzyme HMG-CoA reductase. What would happen to HMG-CoA reductase levels? Again, identify this type of effect and briefly define it.
Cholesterol biosynthesis involves a stepwise increase of carbon numbers from acetyl-CoA (C2) to ______ (C5), and, finally, to squalene (C30). But, the rate-limiting step is catalyzed by _____. Inhibition of this enzyme is adopted as a strategy for the therapeutic control of cholesterol levels. Select one: a. isoprenoid ;;; HMG CoA synthase b. isoprenoid ;;; HMG CoA reductase c. flavonoid ;;; HMG CoA synthase d. flavonoid ;;; HMG CoA reductase e. None of these
Statins work to inhibit cholesterol synthesis by competing for the active site of an enzyme involved in this pathway. What is the normal product of this enzyme? a. Squalene b. Mevalonate c. HMG CoA d. Isopenetnyl pyrophosphate
Statin drugs, like Mevacor (lovastatin) and Lipitor (atorvastatin), act as competitive inhibitors of HMG-CoA reductase by mimicking the structure of mevalonate. However, it is not this inhibition that directly lowers cholesterol levels in the blood. What enzymatic reaction does HMG CoA-reductase catalyze? What is important about this step of cholesterol synthesis? How can statins mechanistically cause a decrease in LDL cholesterol in the blood if it is not a direct effect of decreased cellular cholesterol synthesis?
Which enzyme that participates in ketoacid metabolism is not present in the liver? a) HMG-CoA synthase b)β-ketoacyl CoA transferase c)Thiolase d) β -hydroxybutyrate dehydrogenase
Give the process/pathway where each of the following enzymes is involved: a. HMG CoA lyase b. HMG CoA reductase c. Acetyl CoA carboxylase d. Acyl CoA dehydrogenase