JOEL MOSS, M.D., Ph.D.; DRUSILLA L. BURNS, Ph.D.; JUDITH A. HSIA, M.D.; ERIK L. HEWLETT, M.D.; RICHARD L. GUERRANT, M.D.; MARTHA VAUGHAN, M.D.
In several bacterial diseases, the clinical, laboratory, and histologic findings result from the elaboration by the organism of a toxic product that binds to and may enter the host cell to alter its metabolism. In some cases, the intracellular mediators of toxin action are the cyclic nucleotides, cyclic adenosine 5′-monophosphate (cAMP) and cyclic guanosine 5′-monophosphate (cGMP), the ubiquitous second messengers through which numerous hormones, neurotransmitters, and drugs exert their effects. Certain toxins act by enhancing the activity of cellular enzymes that synthesize cAMP or cGMP; and others, by themselves catalyzing cAMP synthesis after entering the cell. Studies of the mechanism of action of these toxins have helped in deciphering the enzymatic components within animal cells that are responsible for cyclic nucleotide synthesis, degradation, and function as well as in understanding the pathogenesis of the diseases in which they are involved.
MOSS J, BURNS DL, HSIA JA, et al. Cyclic Nucleotides: Mediators of Bacterial Toxin Action in Disease. Ann Intern Med. 1984;101:653–666. doi: 10.7326/0003-4819-101-5-653
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Published: Ann Intern Med. 1984;101(5):653-666.
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