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Section VII – Structure, Function, & Replication of Informational Macromolecules

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Which of the following statements about β,γ-methylene and β,γ-imino derivatives of purine and pyrimidine triphosphates is CORRECT?

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A. They are potential anticancer drugs.

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B. They are precursors of B vitamins.

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C. They readily undergo hydrolytic removal of the terminal phosphate.

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D. They can be used to implicate involvement of nucleotide triphosphates by effects other than phosphoryl transfer.

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E. They serve as polynucleotide precursors.

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β,γ-Methylene and β,γ-imino purine pyrimidine triphosphates do not readily release the terminal phosphate by hydrolysis or by phosphoryl group transfer.

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Which of the following statements about nucleotide structures is NOT CORRECT?

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A. Nucleotides are polyfunctional acids.

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B. Caffeine and theobromine differ structurally solely with respect to the number of methyl groups attached to their ring nitrogens.

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C. A purine is a heterocyclic aromatic molecule composed of a pyrimidine ring fused to an imidazole ring.

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D. NAD+, FMN, S-adenosylmethionine, and coenzyme A all are derivatives of ribonucleotides.

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E. 3′,5′-Cyclic AMP and 3’,5’-cyclic GMP (cAMP and cGMP) serve as second messengers in human physiology.

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Which of the following statements about purine nucleotide metabolism is NOT CORRECT?

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A. An early step in purine biosynthesis is the formation of PRPP (phosphoribosyl 1-pyrophosphate).

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B. Inosine monophosphate (IMP) is a precursor of both AMP and GMP.

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C. Orotic acid is an intermediate in pyrimidine nucleotide biosynthesis.

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D. Humans catabolize uridine and pseudouridine by analogous reactions.

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E. Ribonucleotide reductase converts nucleoside diphosphates to the corresponding deoxyribonucleoside diphosphates.

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Pseudouridine is excreted unchanged in human urine. Its presence there is not indicative of pathology.

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Which of the following statements is NOT CORRECT?

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A. Metabolic disorders are only infrequently associated with defects in the catabolism of purines.

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B. Immune dysfunctions are associated both with a defective adenosine deaminase and with a defective purine nucleoside phosphorylase.

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C. The Lesch-Nyhan syndrome reflects a defect in hypoxanthine-guanine phosphoribosyl transferase.

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D. Xanthine lithiasis can be due to a severe defect in xanthine oxidase.

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