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

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

A. They are potential anticancer drugs.

B. They are precursors of B vitamins.

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

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

E. They serve as polynucleotide precursors.

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

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

A. Nucleotides are polyfunctional acids.

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

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

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

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

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

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

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

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

D. Humans catabolize uridine and pseudouridine by analogous reactions.

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

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

Which of the following statements is NOT CORRECT?

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

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

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

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

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