Why is de novo biosynthesis of purines markedly elevated in patients with a deficiency in hypoxanthine-guanine phosphoribosyl transferase (HGPRT)? 5-Fluoruracil is converted to methotrexate by a DPD deficiency, leading to increased purine biosynthesis. OHGPRT deficiency prevents purine salvage, leading to increased purine biosynthesis to make up for it. HGPRT increases pyrimidine salvage and thereby increases purine biosynthesis as a result. Increased purine biosynthesis is the result of ATP hydrolysis during the production of cyclic AMP.
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- Which of the following regulatory mechanisms will specifically inhibit pyrimidine synthesis (and not also purine synthesis)? (A) allosteric regulation of aspartate transcarbamoylase by CTP(B) allosteric regulation of aspartate transcarbamoylase by ATP(C) synergistic inhibition of PRPP synthetase by AMP/GMP/IMP(D) synergistic inhibition of PRPP amidotransferase by AMP/GMP/IMP (E) feedback inhibition of ribonucleotide reductase by dATPNormal cells die in a nutrient medium containing thymidine and methotrexate, whereas mutant cells defective in thymidylate synthase survive and grow. Explain.The enzymatic activity of PFK1 is generally measured by set- ting up a coupled enzyme assay system whereby aldolase, triose phos- phate isomerase, and glycerol-3-phosphate dehydrogenase are added to the assay mixture. For the latter enzyme, NADH is added and its change in concentration is readily monitored at 340 nm. Write the chain of reactions catalyzed by these enzymes using structural formulas, label substrates and products, and explain why the coupled en- zyme assay system leads to oxidation of NADH. While the chain of reac- tions is similar to those in glycolysis, there is a critical difference because of the dehydrogenase enzyme. Describe how this enzyme causes the chain of reactions to differ from those in glycolysis.
- Bacterial species that are capable of synthesising the amino acid histidine do not need it in their growth medium. Histidine biosynthesis requires a specific enzyme, which we shall refer to as histidine synthetase. When these bacteria are supplemented with histidine in their growth media, they cease intracellular histidine synthesis. Propose three distinct regulatory mechanisms to account for why histidine production ends when histidine is present in the growth medium. To further investigate this phenomena, you analyse the quantity of intracellular histidine synthetase protein produced when cells are cultured with and without histidine. The quantity of this protein is same in both scenarios. Which regulatory mechanism makes sense in light of this observation?Why Phenylmethylsulfonyl fluoride (PMSF, shown in Fig.) does not inhibit aspartate protease as potent as serine protease?Orotic aciduria is a rare hereditary disorder due to deficient orotate phosphoribosyltransferase and orotidine-5'-decarboxylase activities that are encoded by Uridylate (UMP) synthetase gene in de novo pyrimidine biosynthesis. The characteristic of this disorder is excessive excretion of orotic acid in urine. A mutation of UMP synthetase gene has been identified as R96G (at amino acid position 96, Arginine is changed to Glycine). In orotic aciduria, predict the consequences of deficient UMP synthetase by identifying which downstream enzyme missing its action. One of important molecules to be derived from pyrimidine biosynthesis is deoxycytidine triphosphate (dCTP) for DNA replication and repair. How is dCTP synthesized, include what enzymes and important intermediates in the pathway? 3. As thymidine triphosphate (dTTP) is needed for DNA replication and repair, what enzymes and intermediates are required to get dTTP
- What is the relationship between protein modification and allosteric control of phosphofructokinase?Hydroxyurea has been shown to increase the expression of fetal hemoglobin in adult red blood cells, by a mechanism that remains unclear. Explain why hydroxyurea can be a useful therapy for patients with sickle-cell anemia.Why is it advantageous for two control mechanisms —allosteric control and covalent modification— to be involved in the metabolism of glycogen?
- The Energy Cost of dTTP Synthesis (Integrates with Chapter 20.) Starting from HCO3, glutamine, aspartate, and ribosc-5-P, how many ATP equivalents are consumed in the synthesis of dTTP in a eukaryotic cell, assuming dihydroorotate oxidation is coupled to oxidative phosphorylation? How does this result compare with the ATP costs of purine nucleotide biosynthesis calculated in problem 2?what cell types are Hexokinase I and Hexokinase IV found? Explain 2 additional differences (in addition to cell-type specificity) that exist between these two isoenzymes.Does PFK-2 (Phosphofructokinase-2) have coenzymes and Allosteric reguation?