Predict the effect of each of the following mutants on the rate of glycolysis in liver cells (increase, decrease, no change): (a) Loss of the allosteric site for ATP in PFK-1 (b) Loss of the binding site for citrate in PFK-1 (c) Loss of the phosphatase domain of PFK-2/FBPase-2 (d) Loss of the binding site for fructose-1,6-bisphosphate in pyruvate kinase (e) Loss of acetyl-CoA binding site in pyruvate carboxylase

Predict the effect of each of the following mutants on the rate of glycolysis in liver cells (increase, decrease, no change): (a) Loss of the allosteric site for ATP in PFK-1 (b) Loss of the binding site for citrate in PFK-1 (c) Loss of the phosphatase domain of PFK-2/FBPase-2 (d) Loss of the binding site for fructose-1,6-bisphosphate in pyruvate kinase (e) Loss of acetyl-CoA binding site in pyruvate carboxylase

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter27: Metabolic Integration And Organ Specialization

Section: Chapter Questions

Problem 20P: Figure 27.3 illustrates the response of R (ATP-regenerating) and U (ATP-utilizing) enzymes to energy...

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Sketch curves for reaction velocity versus [fructose-6-phosphate] for the phosphorylated and nonphosphorylated forms of PFK-2 in liver.
Concerning the reciprocal regulation of phosphofructokinase and fructose-1,6-bisphosphatase in the liver, which of the following statements are true? Select all that apply A.The default activity of the cell favors activity of phosphofructokinase-2 being activated, generating fructose-2,6-bisphosphate that serves as a potent allosteric activator of phosphofructokinase B.Glucagon binding ensures that the levels of fructose-2,6-bisphosphate drop within the liver cell C.In the presence of ATP and fructose-2,6-bisphosphate, phosphofructokinase will be fully inhibited and glycolysis turned off D.High levels of fructose-2,6-bisphosphate signals for activation of gluconeogenesis and inhibition of glycolysis E.Glucagon binding to the liver cell activates a phosphorylation cascade that inhibits activity of phosphofructokinase-2 and activates fructose-2,6-bisphosphatase F.Glucagon binding activates glycolysis as it signals high blood sugar levels
Neuraminidase (NA) catalyzes a hydrolysis of the glycosidic linkages of sialic acids using a mechanism shown in Fig. (a). and Fig. (b) shows competitive inhibitors of NA Considering the mechanism of NA, why do zanamivir and oseltamivir inhibit NA so potently?
By analysis of the kinetics of interconversion of (1-13C]FBP and [6-13C]FBP and the appearance of 3-PGA and PEP in further experiments such as shown in the figure above, it was concluded that the rate of oxidation of glyceraldehyde-3-phosphate (GAP) was hindered under conditions of anaerobiosis. Separate experiments showed that the activity of 3-phosphoglcerate kinase was normaland that the concentrations of ADP and ATP were not limiting. What metabolic condition is the most likely to account for this conclusion? Write the reaction using structural formulas and naming reactants
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What would be the effect of the Glucagon initiated cascade on inhibition of ATP Synthase by IF1? Metabolic reprogramming in cancer cells correlates to an enhanced expression of IF1. What would be the effect on the TCA? Why might that lead to lactoacidosis?
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. In Figure 6-11,a. in view of the position of HPA oxidase earlier in thepathway compared to that of HA oxidase, would youexpect people with tyrosinosis to show symptoms ofalkaptonuria?b. if a double mutant could be found, would you expecttyrosinosis to be epistatic to alkaptonuria?
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