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Section on Biochemistry of Cell Regulation, Laboratory of Biochemical Pharmacology [E. F. G., G. L., P. S. L., L. D. K.] and Laboratory of Experimental Pathology [R. M. F.], National Institute of Arthritis, Metabolism, and Digestive Diseases, NIH, and Division of Bacterial Products, Bureau of Biologics, Food and Drug Administration, Bethesda, Maryland 20014 [S. R.], and Laboratory of Membrane Biochemistry, Roche Institute of Molecular Biology, Nutley, New Jersey 07110 [H. R. K.]
This report describes similarities between the structure and function of the interferon receptor and receptors for glycoprotein hormones and several bacterial toxins. Specifically, it describes several common molecular and mechanistic elements, including: (a) the presence of a glycoprotein as well as a ganglioside component in the receptor; (b) changes in membrane structure as a consequence of interferon action; (c) interferon-induced intracellular cyclic adenosine 3':5'-monophosphate changes; and (d) alterations in the flux of certain ions across the membrane. Since interferon has an antiviral effect, these results define a relationship between hormonal perturbation of cellular events and the ability of an agent to prevent or suppress viral infections of cells. Further definition of these relationships should be important to our understanding of the oncogenic state, of hormonal effects on the oncogenic state, and of other human diseases in which hormonal perturbations of non-target tissues or cross-reactivity of receptors could be pathogenic.
1 Presented at the John E. Fogarty International Center Conference on Hormones and Cancer, March 29 to 31, 1978, Bethesda, Md.
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