The regulation of Glutamine Synthetase (GS) in E.coli, a model for this highly conserved homodecamer in mammals, and is a striking example of cumulative feedback inhibition through allosteric regulation. Explain the cumulative feedback inhibition of GS..
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The regulation of Glutamine Synthetase (GS) in E.coli, a model for this highly conserved homodecamer in mammals, and is a striking example of cumulative feedback inhibition through allosteric regulation. Explain the cumulative feedback inhibition of GS..
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- cis-Vaccenate is an 18-carbon unsaturated fatty acid abundant in E. coli membrane lipids. Propose a metabolic route for synthesis of this fatty acid, in light of the fact that stearic acid, the C1g saturated analogous fatty acid, is virtually absent from E. coli lipids.Describe two types of regulation of the enzyme glutamine synthetase and explain why the regulation of this enzyme is soooo complex.The mitochondrial form of carbamoyl phosphate synthetase is allosterically activated by N-acetylglutamate. Briefly describe a rationale for this effect.
- Equation 7a of the text, (Umax/KM1) [S] (v'max/KM2) [P] 1+ [S]/KM1 + [P]/KM2 - gives the expression for the rate of formation of product by a modified version of the Michaelis-Menten mechanism in which the second step is also reversible. Derive the expression and find its limiting behaviour for high and low concentrations of substrate.Synthesis of the purine nucleotides AMP andGMP proceeds by a branched pathway starting with ribose5-phosphate (R5P), as shown schematically in FigureQ3–4. Using the principles of feedback inhibition, proposea regulatory strategy for this pathway that ensures an ade-quate supply of both AMP and GMP and minimizes thebuildup of the intermediates (A–I) when supplies of AMPand GMP are adequate.a gain-of-expression of MCT1 transporters in pancreatic b-cells wreaks havoc on the cell’s function. To consider this point further, determine the number of ATP that result from complete catabolism of a) 5 lactate and b) 5 b-hydroxybutyrate in aerobic conditions in humans. Assume TCA intermediates are NOT limiting. Use the exact number of c-subunits and the details of the electron transport chain in humans to determine the number of ATP from NADH and FADH2 (not 2.5ATP per NADH and 1.5ATP per FADH2