Abstract
The main interest of the late Earl Sutherland was to prove or disprove the hypothetical existence of an intracellular regulator which antagonizes the action of cyclic AMP (1). A starting observation was, that following a first stimulation of hepatocytes with glucagon, it was possible to increase cyclic AMP levels also a second time. However, in the case of stimulation with adrenaline, cyclic AMP levels rise only a little bit on a first but not on a second stimulation (Fig. 1). The assumption was that in the latter case the adenylate cyclase has been inhibited by an intracellular regulator, the synthesis of which must have been stimulated following the first stimulation with adrenaline. It is unclear up to now, whether homologous and heterologous desensitization on the one hand and activation of inhibitory G-proteins (Gi) on the other are the only mechanisms by which adenylate cyclase activity is regulated (2). In addition to these mechanisms, there also exists a regulator of low molecular weight, which is a potent inhibitor of adenylate cylase (3,4).
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Wasner, H., Lemoine, H., Junger, E., Leßmann, M., Kaufmann, R. (1991). Prostaglandyl-Inositol Cyclic-Phosphate, A New Second Messenger. In: Bailey, J.M. (eds) Prostaglandins, Leukotrienes, Lipoxins, and PAF. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0727-1_16
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