A child with coarse facies, corneal clouding, joint stiffness and mental retardation is found to have a Damage to this enzyme directly affects which of partial defect in N-acetylglucosaminotransferase. the following biochemical functions? A. Formation of polysomes B. Microtubule attachment to centrioles C. Synthesis of ribosomal RNA D. Targeting of enzymes for lysosomes E. Transport of sugars into mitochondria
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- . In Figure 6-11,a. in view of the position of HPA oxidase earlier in thepathway compared to that of HA oxidase, would youexpect people with tyrosinosis to show symptoms ofalkaptonuria?b. if a double mutant could be found, would you expecttyrosinosis to be epistatic to alkaptonuria?The action of this enzyme found in Beano alpha-galactosidase can also according to many sources be used to remove ____________ from the red blood cells of the B blood group and convert them to the O blood group. Since the _________ molecules (composed of many monomers) are connnected to protein on the membrane and also the cell membrane of the red blood cell itself; therefore these molecules help create cell identity and recognition, and when the are connected to proteins they are known as _________ , but if they are connected to the cell membrane itself they are known as ____________. This is a good question for reviewing the structures on the cell membrane as well. The only difference between the B-blood type and the O-blood type is ________. The following is a diagram of the differences of these molecules that determine blood type. List of answers: disaccharid, proteins ,dehydration synthesis ,nucleotide ,amino acids ,nucleic acids ,lactose ,fructose ,sucrose ,hydrolysis…Which of the following correctly describes the regulation and activity of HIF-1? Group of answer choices VHL is required for preventing degradation of HIF-1alpha and promoting translocation to the nucleus In normoxia, HIF-1alpha is ubquitinated and degraded in the proteasome Hypoxic conditions result in increase hydroxylation of prolines in HIF-1alpha The primary function of HIF-1 is to phosphorylate and activate glycolytic enzymes
- In acute lymphoblastic leukemia, the cancerous white blood cells typically lack the enzyme asparagine synthetase. Why is the administration of asparaginase an eff ective therapy for this type of cancer?TPCK and TLCK are irreversible inhibitors of serine proteases. One ofthese inhibits trypsin and the other chymotrypsin. Which is which? Explainyour reasoning. Suggest the effects of each of the following mutations on the physiologicalrole of chymotrypsinogen:(a) R15S(b) C1S(c) T147SDescribe the mechanism of action of 1 cycle of the ubiquitin (Ub) ligase system. Describe how the E1, E2 and E3 ligases work to covalently link Ub to the target protein, including which uses an energy source (and how), and the operative amino acids on the enzymes, Ub and target protein
- During SDS-PAGE, glycoproteins migrate as relatively diffuse bands, whereas nonglycosylated proteins typically migrate as narrow, well-defined bands. Explain the reason for this difference in electrophoretic behavior.Pompe disease is due to a deficiency in lysosomal α-1,4-glucosidase, also called acid maltase. Lysosomes function as recycling centers in the cell and normally degrade excess muscle glycogen into glucose for the energy-converting reactions of the glycolytic pathway. Pompe disease was described in 1932 by Dutch pathologist Johann Pompe, who recognized that lysosomes in the affected patient's accumulated large amounts of glycogen. However, Henri Hers—the same Belgian pathologist who described the symptoms of liver glycogen phosphorylase deficiency (Hers disease)—discovered in 1965 that Pompe disease was due to a lysosomal α-1,4-glucosidase deficiency. Enzyme deficiency Disease name Organ Disease symptoms Lysosomal α-1,4- glucosidase Pompe All organs Heart failure in infantile form; muscle defects in juvenile form Answer these questions: What protein/enzyme does the mutation effects? Symptoms and, if you can, how are the symptoms…A species of bacteria can synthesize the amino acid histidine, so they do not require histidine in their growth medium. A key enzyme, which we will call histidine synthetase, is necessary for histidine biosynthesis. When these bacteria are given histidine in their growth medium, they stop synthesizing histidine intracellularly. Based on this observation alone, propose three different regulatory mechanisms to explain why histidine biosynthesis ceases when histidine is in the growth medium. To explore this phenomenon further, you measure the amount of intracellular histidine synthetase protein when cells are grown in the presence and absence of histidine. In both conditions, the amount of this protein is identical. Which mechanism of regulation is consistent with this observation?
- Tissues that are unable to produce nucleotides de novo depend on ____________________ to maintain an adequate supply of adenine nucleotides. (A) the redox reactions carried out by ribonucleotide reductase (B) the action of PRPP amidotransferase(C) uptake of ATP through dietary intake(D) salvaging hypoxanthine using HGPRT (E) the action of xanthine oxidaseIdentify the following by describing their functions: EF-G, EF-Tu, EF-Ts, EF-P, and peptidyl transferaseWhich of the following would be a good chemotherapy approach: blocking formationof the ribonucleotide GTP or blocking formation of the deoxyribonucleotide dGTP?Why? Please explain the chemical differences between each of the two nucleotides. Use the specific processes below to support your choice by explaining how either GTP or dGTPare related to these and how loss of the particular molecule would affect each process. *PEP carboxykinase in gluconeogenesis*Succinyl-CoA synthetase in the TCA Cycle*Glucagon signal transduction