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- 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) T147SWhat effect does binding of the IRF protein to the IRE in the mRNA encoding ferritin have on the production of ferritin? Briefly explain why this effect is observed.The lac genotypes are as shown below: P+OcZ-Y+A+// P¯O+Z+Y+A+ (i) The lac operon consists of three structural genes, lacZ, lacY and lacA. Which structural genes are involved in lactose metabolism? Explain. (ii) Draw and explain how lactose repress the gene expression in lac IS/I- heterozygote. (iii) What is the function of the promoter in the bacterial operon?
- A genetic defect in coagulation factor IX causes hemophilia b, a disease characterized by a tendency to bleed profusely after very minor trauma. However, a genetic defect in coagulation factor XI has only mild clinical symptoms. Explain this discrepancy in terms of the mechanism for activation of coagulation proteases shown in Box.The enzyme glucose oxidase isolated from the mold Penicillium notatum catalyzes the oxidation of β-Dglucose to D-glucono-δ-lactone. This enzyme is highly specific for the β anomer of glucose and does not affect the α anomer. In spite of this specificity, the reaction catalyzed byglucose oxidase is commonly used in a clinical assay for total blood glucose—that is, for solutions consisting of a mixture of β- and α-D-glucose. What are the circumstances required to make this possible? Aside from allowing the detection of smaller quantities of glucose, what advantage does glucose oxidase offer over Fehling’s reagent for measuring blood glucose?Why Phenylmethylsulfonyl fluoride (PMSF, shown in Fig.) does not inhibit aspartate protease as potent as serine protease?
- The enzyme glucose oxidase isolated from the mold Penicillium notatum catalyzes the oxidation of B-D-glucose to D-glucono-6-lactone. The enzyme is highly specific for the B anomer of glucose and does not affect the a anomer. In spite of this specificity, the reaction catalyzed by glucose oxidase is commonly used in a clinical assay for total blood glucose -that is, for solutions consisting of a mixture of B- and a-D-glucose, as well as other sugars present in blood. The oxidation proceeds in the presence of oxygen and forms hydrogen peroxide, in addition to the lactone. A second enzyme, called peroxidase, catalyzes the reaction of hydrogen peroxide with colorless compounds to create a colored product, which is quantified with a simple spectrophotometer. What are the circumstances required to make this possible? Aside from allowing the detection of smaller quantities of glucose, what advantage does glucose oxidase offer over the Fehling's reagent for measuring blood glucose?A number of auxotrophic mutant strains were isolated from wild-type haploid Neurospora crassa. These strains responded to the addition of certain nutritional supplements to minimal culture medium either by growth (+) or no growth (0) The data from this experiment are presented in the table below. Diagram a biochemical pathway, complete with positions of intermediates, that is consistent with the data. Indicate where in the pathway each mutant strain is blocked.Would the following alterations to Src be oncogenic? Explain. (a) The mutation of Tyr 527 to Phe. (b) The replacement of Src residues 249 to 253 with the sequence APTMP.
- TLCK and TPCK both use Histadine residues in the active site as inhibitors of serine proteases. Why is TLCK specific for trypsin and TPCK is specific for chymotrypsin?For each of the E. coli strains that follow, indicate theeffect of the genotype on the expression of the trpEand trpC genes in the presence or absence of tryptophan. [In the wild type (R+ P+ o+ att+ trpE+ trpC+),trpC and trpE are fully repressed in the presence oftryptophan and are fully expressed in the absence oftryptophan.]R = repressor gene; Rnproduct cannot bind tryptophan; R− product cannot bind operatoro = operator for the trp operon; o− cannot bind repressoratt = attenuator; att− is a deletion of the attenuatorP = promoter; P− is a deletion of the trp operonpromotertrpE− and trpC− are null (loss-of-function) mutationsa. R+ P− o+ att+ trpE+ trpC+b. R− P+ o+ att+ trpE+ trpC+c. RnP+ o+ att+ trpE+ trpC+d. R− P+ o+ att− trpE+ trpC+e. R+ P+ o− att+ trpE+ trpC−/R− P+ o+ att+trpE− trpC+f. R+ P− o+ att+ trpE+ trpC−/R− P+ o+ att+trpE− trpC+g. R+ P+ o− att− trpE+ trpC−/R− P+ o− att+trpE− trpC+Measure the uptake of leucine by epithetial cells of the mouse intestine. Measurements of the rate of update of L-leucine, D-Leucine, and L-valine , with and without Na+ in the assay were perform and yield different results (see table below). A) What can you conclude about the properties and mechanism of leucine transporter? B) Would you expect L-leucine uptake to be inhibited by Ouabain, which is a cardiac glycoside drug treatment?