Acyl CoA synthetase hydrolyzes ATP to AMP + PPI (pyrophosphate) as part of the activation of fatty acids to fatty acyl-CoA. Explain the role played by the enzyme inorganic pyrophosphatase in this reaction (in the activation of fatty acids to fatty acyl CoA) in the space provided below.
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Question::
Acyl CoA synthetase hydrolyzes ATP to AMP + PPI (pyrophosphate) as part of the activation of fatty acids to fatty acyl-CoA. Explain the role played by the enzyme inorganic pyrophosphatase in this reaction (in the activation of fatty acids to fatty acyl CoA) in the space provided below.
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- Indicate what will happen (increase, decrease or no effect) to the activity of enzyme or rate of the metabolic pathway given the following conditions: 1. epinephrine to the activity of glycogen synthase 2. high [2-carboxyarabinitol-1-phosphate] to the carboxylase activity of RuBisCOIn working skeletal muscle under anaerobic conditions, glyceraldehyde 3-phosphate is converted to pyruvate (the payoff phase of glycolysis), and the pyruvate is reduced to lactate. Write balanced biochemical equations for all the reactions in this process, with the standard free-energy change for eachreaction. Then write the overall or net equation for the payoff phase of glycolysis (with lactate as the end product), including the net standard free-energy change.a. Some of the acetyl-CoA used in the citric acid cycle is produced from pyruvate. List the reactants and products of this reaction. The reactants are pyruvate and The products are acetyl-CoA and In the process, a(n) is to b. Name an enzyme complex that catalyzes this reaction and list its negative effectors. is the enzyme complex that catalyzes this reaction. Its negative effectors are and
- Arrange the balanced biochemical equations for all the reactions in the catabolism of glucose to two molecules of glyceraldehyde 3-phosphate (the preparatory phase of glycolysis). First step Last step Answer Bank Fructose 1,6-bisphosphate - dihydroxyacetone phosphate + glyceraldehyde 3-phosphate Fructose 6-phosphate + ATP →→→→ fructose 1,6-bisphosphate + ADP Glucose + ATP → glucose 6-phosphate + ADP Dihydroxyacetone phosphate glyceraldehyde 3-phosphate Glucose 6-phosphate →→→→ fructose 6-phosphatephosphofructokinase is an allosteric enzyme that catalyzes the conversion of fructose 6-phosphate to fructose 1,6-bisphosphate and represents the key control point in mammalian glycolysis. The enzyme is a homotetramer that is inhibited by ATP binding, activated by AMP binding, negatively regulated by phosphorylation, and competitively inhibited by 2,5-anhydro-D-glucitol-1,6-diphosphate. (a) Would you expect a plot of the initial rate of fructose 1,6-bisphosphate formation as a function of substrate concentration to show a sigmoidal or hyperbolic curve? (b) How would each of the regulators above affect the dynamics of the T state to R state equilibrium of phosphofructokinase? Briefly explain your reasoning. (c) If it were possible to isolate phosphofructokinase monomers in an active form, how would you expect the kinetics in (a) to be affected? How would the rate of the reaction be affected by ATP, AMP, and 2,5-anhydro-D-glucitol-1,6-diphosphate? Briefly explain your answers.In relation to Carbamoyl Phosphate Synthetase enzyme, answer the following: A- What are the two isoforms of this enzyme, explain why there are two isoforms? B- What are the clinical manifestations associated with the deficiency of these two enzymes? C- Write down the biochemical reaction and the name of the metabolic pathway that these two isoforms are involved in, and how many ATP is utilized by these two isoforms?
- A. The inhibitor constants for three inhibitors of por- cine citrate synthase are summarized in the table on the right. The compounds were all determined to bind in the active site as competitive inhibitors of acetyl-CoA. Because they bind as competitive inhibitors, all three inhibitors must exhibit structural similarity to some part of acetyl-CoA. Look up in the textbook the structural formu- las for Coenzyme A, ATP, and NADH. What is the largest structural fragment of each inhibitor that is responsible for competitive inhibition? Draw the molecular fragment common to each inhibitor that competes with the binding of acetyl-CoA in the active site of citrate synthase. Bromoacetyl-CoA ATP NADH K₁ (μM) 25.7 6800 8300 B While the inhibitor constants listed in part (b) above were determined in vitro for purified citrate synthase, does their inhibitory action have any relevance to the flux of metabolites through the TCA cycle in vivo? If so, explain.Palmitoleic acid, 16:1Δ⁹ hexadecaenoic acid, (16 carbon FA with one double bond )is an important fatty acid component of TAGs and cell membranes. Briefly explain the process of beta oxidation of this fatty acid and the number (only) of FADH, NADH and acetyl CoA outcome. What is the total ATP (only number) generated from this fatty acid after beta oxidation.The clinical signs of two types of galactosemia—galactokinase deficiency or UDPglucose: galactose 1-phosphate uridylyltransferase deficiency—are markedly different. Although both forms cause gastrointestinal pain after drinking milk, transferase deficiency also causes liver, kidney, spleen, and brain malfunction, as well as mortality. With each kind of enzyme shortage, what products accumulate in the blood and tissues? Estimate the relative toxicity of these goods based on the information provided above.
- The clinical symptoms of two forms of galactosemia—deficiency of galactokinase or of UDPglucose: galactose 1-phosphate uridylyltransferase—show radically different severity. Although both types produce gastric discomfort after milk ingestion, deficiency of the transferase also leads to liver, kidney, spleen, and brain dysfunction and eventual death. What products accumulate in the blood and tissues with each type of enzyme deficiency? Estimate the relative toxicities of these products from the above information.During glycogen synthesis, glucose-1P is converted into a molecule called UDPG. This reaction also cleaves uridine triphosphate (UTP) forming uridine monophosphate and pyrophosphate (PPi). Provide four reasons why UTP can be used to power this reaction (no diagrams necessary).19) Consider the table of allosteric effectors and their effect on the following metabolic processes. Glycolysis Gluconeogenesis PDH complex Krebs cycle acetyl-CoA Not applicable AMP Not applicable + glucagon Not applicable Not applicable - Each row contains one error. Correct the error in the table below Table 2 Correction (indicate process and effect (+ or -) acetyl-CoA AMP glucagon - Briefly explain the effect of each allosteric effector on the corrected pathway (based on Table 2 above)