Zidovudine and Stavudine are nucleoside reverse transcriptase inhibitors which consists of a deoxythymidine analogue. Show an outline of a general synthetic protocol to produce an analogue within this series.
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- A conjugate was incubated with a mixture of lysosomal enzymes and no drug release was observed in these conditions. The same conjugate was tested for antitumor activity in vivo and an anticancer effect was observed. Taking into account the information provided above, hypothesize a possible mechanism of action for this conjugate.Among the following structures, the drug that can be given orally against B-lactamase-producing strain: is: CO-H OCH COOH I COOH II NH2 HO COOH III IV COOH Oll ONone of the above OlI OIVCTP synthetase catalyzes the glutamine-dependent conversion of UTP to CTP. The enzyme is allosterically inhibited by the product, CTP. Mamma- lian cells defective in this allosteric inhibition are found to have a complex phenotype: They require thymidine in the growth medium, they have unbal- anced nucleotide pools, and they have an elevated spontaneous mutation rate. Explain the likely basis for these observations.
- Emtricitabine (2',3'-dideoxy-5-fluoro-3'-thiacytidine, abbreviated as FTC) is a nucleoside analog that is used to treat HIV. It works by reversibly binding to HIV reverse transcriptase (HIV RT) and by doing so, inhibits the virus from replicating itself. In an experiment, FTC and purified HIV RT are mixed at low concentrations and allowed to reach equilibrium. The concentrations measured are [FTC] = 10 nM, [HIV RT] = 37.5 nM, and [HIV RT-FTC] = 2.5 µM, for the equilibrium FTC + HIV RT= HIV RT-FTC. What is the Kd in nM?ADH1A alcohol dehydrogenase 1A (class I) Describe a way in which the gene can be manipulated to treat the disease. Assume you can make any changes to the protein product and describe specifically how it will affect its interaction with other molecules.CTP synthetase catalyzes the glutamine-dependent conversion of UTP to CTP. The enzyme is allosterically inhibited by the product, CTP. Mammalian cells defective in this allosteric inhibition are found to have a complex phenotype: They require thymidine in the growth medium, they have unbalanced nucleotide pools, and they have an elevated spontaneous mutation rate. Explain the likely basis for these observations.
- Identify possible sequences of both overdoses and underdoses of amoxicillin.Given the following complementation chart for holes in Monstera, give me the biochemical (phenotype) pathway. A В D E Holes Class 1 + + + - - Class 2 + + Class 3 + + + Class 4 Class 5 + + - - + +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
- Mutants of Neurospora crassa that lack carbamoyl phosphate synthetase I (CPS I) require arginine in the medium in order to grow, whereas mutants that lack carbamoyl-phosphate synthetase II (CPS II) require a pyrimidine, such as uracil. A priori, one would expect the active CPS II in the arginine mutants to provide sufficient carbamoyl phosphate for arginine synthesis, and the active CPS I in the pyrimidine mutants to "feed" the pyrimidine pathway. Explain these observations.A classic way to isolate thymidylate synthase–negative mutants of bacteriais to treat a growing culture with thymidine and trimethoprim. Most ofthe cells are killed, and the survivors are greatly enriched in thymidylatesynthase–negative mutants.(a) What phenotype would allow you to identify these mutants?(b) What is the biochemical rationale for the selection? (That is, why are themutants not killed under these conditions?)(c) How would the procedure need to be modified to select mammalian cellmutants defective in thymidylate synthase?Determine the sequence of a polypeptide treated with trypsin and chimotripsine. Below are the fragments generated with each treatment. Determine the original sequence for both fragmentations (reduerde that they must be equal in the order of amino acids) Quimotripsina 1. Leu-His-Lys-Gln-Ala-Asn-Gln-Ser-Gly-Gly-Gly-Pro-Ser 1. Gln-Gln-Ala-Gln-His-Leu-Arg-Ala-Cys-Gln-Gln-Trp 2. Arg-lle-Pro-Lys-Cys-Arg-Lys-Phe Trypsin 1. Arg 2. Ala-Cys-Gln-GIn-Trp-Leu-His-Lys 3. Cys-Arg 4. Gln-Ala-Asn-Gln-Ser-Gly-Gly-Gly- Pro-Ser 5. lle-Pro-Lys 6. Light 7. Phe-Gin-Gln-Ala-Gln-His-Leu-Arg