Abstract
Although the general contributions of phospholipids to membrane structure and function are now becoming reasonably well understood, there are still relatively few situations in which one can confidently point to a correlation between a specific metabolic or structural characteristic of an individual lipid and a specific membrane function. However, one of the few very clear indications that individual phospholipids can display highly individual behaviour was provided many years ago by Hokin and Hokin (1) when they discovered that in the pancreas acetylcholine and pancreozymin greatly stimulated the incorporation of 32Pi into phosphatidylinositol (PI), a quantitatively minor anionic membrane phospholipid. Since that time a similar ‘phosphatidylinositol response’ has been observed in cells exposed to some, but not all, of the extracellular stimuli that interact with receptors on cell surfaces. Despite this, there is still no single accepted view on the function of this response in the overall pattern of events brought about by cell stimulation. We have recently developed a hypothesis which proposes that the PI response is intimately involved in the functioning of a variety of cell-surface receptor systems which control cell-surface permeability to Ca2+ ions (2–5). This paper will review the evidence relating to this hypothesis and will speculate briefly on how PI breakdown might be implicated in the control of cell surface Ca2+ gates.
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Michell, R.H., Jafferji, S.S., Jones, L.M. (1977). The Possible Involvement of Phosphatidylinositol Breakdown in the Mechanism of Stimulus-Response Coupling at Receptors which Control Cell-Surface Calcium Gates. In: Bazán, N.G., Brenner, R.R., Giusto, N.M. (eds) Function and Biosynthesis of Lipids. Advances in Experimental Medicine and Biology, vol 83. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3276-3_41
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