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- Which of the following tumor-promoting (oncogenic) proteins promotes increased uptake of glutamine? Group of answer choices Pyruvate dehydrogenase kinase Myc GLUT1 HIF-1 Which of the following has the greatest capacity for ATP production by aerobic respiration? fast twitch muscle slow twitch muscle white fat brown fat Which of the following is an inhibitor of Complex I? Azide UCP1 Catalase Rotenone Which of the following facilitates electron transfer from a 2 electron carrier to a 1 electron carrier? Complex II Complex I Complex III Complex IVFor each of the following proteins describe how the protein function would be altered (or not) in the following scenarios: A receptor tyrosine kinase that always dimerizes even in the absence of ligand 3-ketoacyl-CoA transferase (SCOT) that is expressed in the liver. CPT1 that doesn’t have a malonyl binding site 4. acylCoA dehydrogenase with complex V inhibitedWhat is the effect of a defective a(1→ 4) phosphatase in Pompe's disease (GSD II)? O Accumulation of abnormal, unbranched glycogen, leading to heart or liver failure and short fife expectancy O Glycogen accumulation in heart, leading to heart failure, muscle weakness, short life expectancy O Absence of UDP-glucose conversion to glycogen, leading to lack of muscle glycogen, exercise intolerance Glycogen accumulation due to lack of glucose-6-phosphate conversion to glucose, leading to liver enlargement, hypoglycemia, short life expectancy O Lack of complete degradation of glycogen to glucose. leading to mild hypoglycemia, enlarged liver and muscle weakness Submit Request Answer
- phosphofructokinase 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 animal tissues, the ratio of active, unphosphorylated to inactive, phosphorylated pyruvate dehydrogenase (PDH) complex regulates the rate of pyruvate conversion to acetyl‑CoA. Choose an answer in the brackets to finish the sentences. Treatment of a preparation of rabbit muscle mitochondria containing the PDH complex with pyruvate dehydrogenase kinase, ATP, and NADH causes the rate of this reaction to [decrease, increase, stay the same] Treatment of a preparation of rabbit muscle mitochondria containing the PDH complex with pyruvate dehydrogenase phosphatase and Ca2+Ca2+ causes the rate of this reaction to [decrease, increase, stay the same] Treatment of a preparation of rabbit muscle mitochondria containing the PDH complex with malonate causes the rate of this reaction to [decrease, increase, stay the same]Phosphorylation can be inactivating or activating. If oxidation of fatty acids is the primary energy supply being used (low insulin, high glucagon), then acetyl COA with rising concentration is being produced independently of PDC. Would PDCK be active or inactive under these conditions? O The kinase will be active The kinase will be inactive Oxidation of fatty acids won't affect PDC O All of the above
- Between your evening meal and breakfast, your blood glucose drops and your liver becomes a net producer rather than a consumer of glucose. Which statements describe the hormone-stimulated process that triggers glucose production by the liver? The increase in (CAMP] causes protein kinase A to phosphorylate pyruvate kinase, thus inhibiting glycolysis in muscle tissue to promote gluconeogenesis in the liver. The decrease in [fructose 2,6-bisphosphate] stimulates FBPase-1, the key enzyme in gluconeogenesis. Epinephrine stimulates an enzyme cascade involving hepatic protein kinase A (PKA) and phosphorylase b kinase, which eventually leads to glycogen breakdown in the liver. O The rapid decrease in blood glucose levels triggers glucagon release by the pancreas. Glucagon stimulates CAMP-dependent phosphorylation of PFK-2/FBPase-2, which decreases [fructose 2,6-bisphosphate]. The decrease in [fructose 2,6-bisphosphate] stimulates PFK-1, the key enzyme in gluconeogenesis.Discuss the metabolic rationale for phosphorylation of acetyl-CoA carboxylase by AMP-activated protein kinase (AMPK) and cyclic AMP-dependent protein kinase (PKA).Metformin is a commonly used treatment for type 2 diabetes. The active compound was isolated from the french lilac plant and was first used in the 1770s to treat individuals with excessive thirst and frequent urination (LaMoia & Shulman, 2020). Its exact mechanism of action is still under debate, but it ultimately works to lower blood glucose levels. Which of the following proposed mechanisms could explain how metformin works? O inhibits the function of liver glycogen synthase, an enzyme involved in glycogenesis O increases the release of glucagon by the pancreas O decreases gluconeogenesis in the liver O inhibits the breakdown of triglycerides in adipose tissue
- Pyruvate dehydrogenase kinase is a deffected enzyme and it is the connection between the alteration of metabolism and cancer. How the structure and action of this deffective enzyme/protein are altered or essential. This may include the regulation of this protein, its rate of synthesis, importance in rapid cell growth, etc. How does this alteration lead to cancer, enhance the survival of a cancerous cell, etc.? Any pharmaceutical treatments that are in development to target this protein, along with their biochemical basis. Show the chemical structures of any drugs that are discuss as well as their mechanism of action.Pyruvate dehydrogenase kinase-4 (PDK-4) is a widely expressed isoform of PDK and is responsible for inhibiting pyruvate dehydrogenase (PDH) complex activity via phosphorylation. When PDK-4 is active, the PDH complex is in its phosphorylated state and pyruvate cannot be converted into acetyl-CoA for entry into the citric acid cycle. Instead, in gluconeogenic tissues like liver and kidney, pyruvate is channeled to support gluconeogenesis. Conversely, when PDK-4 is inactive, the PDH complex readily converts pyruvate into acetyl-CoA. A researcher wants to determine the role of PDK-4 on blood glucose homeostasis. To accomplish this, she proposes to generate a PDK-4 knockout mouse using CRISPR technology. To create the knockout mouse, she must first generate PDK-4 knockout embryos to implant into pseudopregnant female mice. Arrange the steps to outline the process by which she will generate the PDK-4 knockout embryos. First step Last step Answer Bank Generate Cas9 mRNA and sgRNA specific to…1. The second high energy intermediate metabolite of glycolysis that can be used for substrate level phosphorylation is also a precursor molecule for the synthesis of several amino acids. Name 5 of these amino acids. 2. Explain the indirect effect that allosteric effectors have on pyruvate dehydrogenase activity through phosphorylation/dephosphorylation of components within the PDH-complex.