Hexokinase in red blood cells has a Michaelis constant (KM) of approximately 50 μM. Because life is hard enough as it is, let'sassume that hexokinase displays Michaelis-Menten kinetics.What concentration of blood glucose yields an initial velocity(V) equal to 90% of the maximal velocity (Vmax)?[glucose] =What does the calculated substrate concentration at 90% Vmax tell you if normal blood glucose levels range betweenapproximately 3.6 and 6.1 mM?Hexokinase operates near Vmax only when glucose levels are low.Hexokinase normally operates far below Vmax.Hexokinase operates near Vmax only when glucose levels are high.Hexokinase normally operates near VmaxmM

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Answered: Hexokinase in red blood cells has a…

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter25: Nitrogen Acquisition And Amino Acid Metabolism

Section: Chapter Questions

Problem 22P

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Energetics of the Hexokinase Reaction The standard-state free energy change. Gfor the hexokinase reaction, is â€” 1 6.7 kJ/mol. Use the values in Table I to calculate the value of Gfor this reaction in the erythrocyte at 37Â°C.
Using the Nernst equation, calculate the equilibrium potential for Ca2 and for C1 from the following sets of data: a. Given [ Ca2+ ]0=1mM,[ Ca2+ ]i=100nM, find Eca2+ b. Given [ Cl- ]0=110mM,[ Cl- ]i=100mM, find Ecl
Using the ActiveModel for enoyl-CoA dehydratase, give an example of a case in which conserved residues in slightly different positions can change the catalytic rate of reaction.
Understanding the Mechanism of Hemolytic Anemia Genetic defects in glycolytic enzymes can have serious consequences for humans For example, defects in the gene for pyruvate kinase can result in a condition known as hemolytic anemia. Consult a reference to learn about hemolytic anemia, and discuss why such genetic defects lead to this condition.
The Catabolism of Uric Acid Write a balanced equation for the oxidation of uric acid to glyoxylic acid, CO2, and NH3, showing each step in the process and naming all of the enzymes involved.
Distinguishing the Mechanisms of Class I and Class I Aldolases Fructose bisphosphate aldolase in animal muscle is a class 1 aldolase, which forms a Schiff base intermediate between substrate (for example. fructose-1, 6-bisphosphate or dihydroxyacetone phosphate) and a lysine at the active site (see Figure I8.12). The chemical evidence for this intermediate conies from studies with aldolase and the reducing agent sodium borohydride, NaBH4. Incubation of the enzyme with dihydroxyacetone phosphate and NaBH4 inactivates the enzyme. Interestingly, no inactivation is observed if NabH4 is added to the enzyme in the absence of substrate. Write a mechanism that explains these observations and provides evidence for the formation of a Schiff base intermediate in the aldolase reaction.
Extending the Mechanism of Methylmalonyl-CoA Mutase to Similar Reactions Based on the mechanism for the methylmalonyl-CoA mutase (see problem 14), write reasonable mechanisms for the following reactions shown.
The Reactions and Meehanisms of the Leloir Pathway Write the reactions that permit galactose to be utilized in glycolysis. Write a suitable mechanism, tor one of these reactions.
Using the ActiveModel for aldose reductase, describe the structure of the TIM barrel motif and the structure and location of the active site.
Characterizing Glycolysis List the reactions of glycolysis that a. are energy consuming (under standard-stale conditions), b. are energy yielding (under standard-state conditions), c. consume ATP. d. yield ATP e. are strongly influenced by changes in concentration of substrate and product because of their molecularity. f. are at or near equilibrium in the erythrocyte (see Table 18.2).
Effects of Changing Metabolite Concentrations on Glycolysis In an erythrocyte undergoing glycolysis what would be the effect of a sudden increase in the concentration of a. AÎ¤P? b. AMP? c. fructose-1.6-bisphosphate? d. fructose-2, 6-bisphosphate? e. citrate? f. glucose-6-phospthate?
If phenylalanine was not an essential amino acid, would diet therapy (the elimination of phenylalanine from the diet) for PKU work?

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