Abstract
In a scant few years, the ligand-stimulated turnover of phosphatidylinositol (PI) has progressed from a curious observation to a major biochemical and pharmacological enterprise. In the 1940’s, de Hevesy (see de Hevesy, 1964) introduced the use of beta-emitting radioisotopes to biochemistry, and demonstrated that the addition of 32P-labeled inorganic phosphate to tissue preparations led to highly radioactive phospholipids. In 1953, Hokin and Hokin published their seminal observation that two minor phospholipids, phosphatidylinositol (PI) and phosphatidate (PA) were selectively labeled to high specific activities in such preparations (Hokin and Hokin, 1953). Furthermore, the labeling was greatly intensified by the presence of cholinergic ligands in the incubation medium, and the stimulated labeling could be reduced to the basal level by the addition of atropine, a known antagonist of muscarinic cholinergic receptors. This latter observation was important, since it demonstrated that the stimulated labeling is indeed receptor-linked. Hence their observation constituted a biochemical “handle” into the transduction process whereby a receptor-ligand interaction on the outer leaflet of the plasma membrane is converted to an intracellular response. Over the intervening years, it became apparent that a large number of receptor-ligand interactions could be coupled to stimulated PA and PI labeling, and that they formed a class distinct from receptor-ligand interactions linked to cyclic AMP.
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Agranoff, B.W. (1987). Receptor-Mediated Phosphoinositide Metabolism. In: Ehrlich, Y.H., Lenox, R.H., Kornecki, E., Berry, W.O. (eds) Molecular Mechanisms of Neuronal Responsiveness. Advances in Experimental Medicine and Biology, vol 221. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7618-7_5
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