Glycolysis is regulated by the enzyme phosphofructokinase 1 (PFK), which catalyzes the formation of fructose 1,6 bisphosphate. In bacteria, PFK is a 300 amino acid protein. If a nonsense mutation occurred at amino acid 50, which of the following would you expect? The amount of fructose 1,6 bisphosphate would be unchanged Glucose levels would decrease Glycolysis would stop functioning More fructose 1,6 bisphosphate would be formed Pyruvate levels would increase
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- Which of the following is likely to be correct if all mutases are completely inhibited?a. Removal of glucosyl residues from nonreducing ends of glycogen in the liver is compromised;therefore, release of free glucose into blood from the liver would decreaseb. Glycerol can be efficiently converted into glucose but cannot be efficiently converted into glucosylresidues in glycogen in the liverc. Bothaandbd. Neither a nor bThe M and H subunits of lactate dehydrogenase have very similar sizes and shapes but differ in amino acidcomposition. If the only difference between the two were that theH subunit had a glutamic acid in a position where the M subunithad a serine, how would the five isozymes of LDH separate on electrophoresis using a gel at pH 8.6?Which of the following coenzymes are required for the metabolic reactions that convert glycerol intoglucose? NAD+ Biotin Both A and B Neither A nor B Assume that the gene for glycogen phosphorylase kinase is mutated and the mutated enzyme cannotbe phosphorylated. Which of the following statements applies to individuals carrying such a genemutation? -Glycogen phosphorylase becomes less active -More glycogen phosphorylase b is converted to glycogen phosphorylase a - Both A and B - Neither A nor B
- Which of the following components of the ubiqutin-proteasome pathway are ATPases? (i.e., which consume ATP in order to function?) (Select all that apply) a)E3 ubiquitin-protein ligase b)19S proteasome c)20S proteasome d)E2 ubiquitin-conjugating enzyme e)E1 ubiquitin-activating enzyme f)UbiquitinAll are single-electron carriers EXCEPT: a. UQH2. b. Cyt bL. c. Cyt bH. d. Rieske protein Fe-S clusters. e. Cyt c1. 2.The energy input for the synthesis of glycogen occurs during which of the following enzyme catalysed steps? a. phosphoglucomutase b. UDP-glucose pyrophTosphorylase c. glycogen synthase d. amylo-(1,4®1,6)-transglycosylase e. none of the above require energy input ______________________________________________________________________________(What is the smallest number of molecules of ATP and GTP consumed in the synthesis of a 200- residue protein, starting from amino acids? Assume that the hydrolysis of PP i is equivalent to the hydrolysis of ATP for this calculation.
- Predict the effect of each of the following mutations on the pace of glycolysis in liver cells: (a) Loss of the allosteric site for ATP in phosphofructokinase (b) Loss of the binding site for citrate in phosphofructokinase (c) Loss of the phosphatase domain of the bifunctional enzyme that controls the level of fructose 2,6-bisphosphate (d) Loss of the binding site for fructose 1,6-bisphosphate in pyruvate kinaseWhat would be the effect on an organism’s ability to use glucose as an energy source if a mutation inactivated glucose 6-phosphatase in the liver?Leigh syndrome is characterized by psychomotor regression: that is, the progressive loss of mental andmovement abilities. Patients also suffer from lacticacidosis, a condition in which mitochondrial respiration is deficient, so their tissues metabolize glucoseanaerobically, leading to the buildup of lactate. Somepatients with Leigh syndrome have a mutation in themitochondrial gene MT-CO3, which encodes a subunit of the electron transport complex cytochromec oxidase. Other patients diagnosed with Leigh syndrome have a loss-of-function mutation in the nucleargene SURF1, which encodes a factor needed for theassembly of this same enzyme complex.a. How can the same symptoms result from mutationsin a mitochondrial gene and from mutations in anuclear gene?
- The normal enzyme required for converting sugars into glucose is present in cells, but the conversion never takes place and no glucose is produced. What could have occurred to cause this defect in a metabolic pathway?Will the amount of glycogen be higher or lower than normal or unchanged? Pyridoxal phosphate is covalently bonded to glycogen phosphorylase via a Schiff base to Lys 680. What effect would the mutation of Lys680Ala have on the breakdown of glycogen?(This notation means the following: K680 is the normal amino acid in this enzyme. It has been mutated to 680A.) Loss of the gene for the kinase that phosphorylates GSK3 on glycogen synthesis. Effect of the substrate analog below on glycogen synthesis.The complete oxidation of glucose 6-phosphate derived from free glucose yields 30 molecules ATP, whereas the complete oxidation of glucose 6- phosphate derived from glycogen yields 31 molecules of ATP. Account for this difference.