Abstract
Twenty years ago an enzyme hydrolyzing phosphatidylinositol by the phospholipase C route was first reported (Kemp et al., 1959) and shown to be activated by calcium ions. The products of the reaction are diacylglycerol and inositol phosphate. Subsequent work has shown that the enzyme is widely distributed in mammalian tissues and that it is the key enzyme in what has been called the ‘phosphatidylinositol effect’ (Hokin & Hokin, 1953). This is the increased turnover of phosphatidylinositol, often measured by 32P incorporation, in response to activation of various types of plasma membrane receptors. For recent reviews, see Michell (1975) and Hawthorne and Pickard (1979). The physiological significance of the effect remains uncertain, though Michell and others believe that it is associated with calcium gating (Michell et al., 1977 Berridge & Fain, 1979). A conference volume presents other points of view (Wells & Eisenberg, 1978). Our purpose here is not to discuss why the effect is there. Instead we shall consider what part the phospholipase C might play, since it is reasonable to assume that phosphatidylinositol effect always begins with this enzyme.
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Hawthorne, J.N., Pickard, M. (1980). Phosphatidylinositol as a Source of Diacylglycerol to Promote Membrane Fusion in Exocytosis. In: Kates, M., Kuksis, A. (eds) Membrane Fluidity. Experimental Biology and Medicine, vol 1. Humana Press. https://doi.org/10.1007/978-1-4612-6120-9_20
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DOI: https://doi.org/10.1007/978-1-4612-6120-9_20
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