Abstract
Phosphatidylinositol (PI), PI-4-phosphate (PIP) and PI-4, 5-bisphosphate (PIP2) have drawn a great deal of attention mainly because of their key role in agonist-induced transmembrane signal transduction (Berridge and Irvine, 1989; Williamson and Hansen, 1987). Activation of receptors may lead to phospholipase C-dependent degradation of PIP2 and the formation of inositol 1,4, 5-trisphosphate and diglyceride as second messengers. In order to maintain the levels of hormone-sensitive PIP2 in the plasma membrane, phosphorylation reactions occur that convert PI into PIP2. PI- and PIP kinases involved in these reactions, are most likely active at the level of the plasma membrane. As a result, the plasma membrane PI-pool will be depleted. Since de novo synthesis of PI does not occur in the plasma membrane (Lundberg and Jergil, 1988 Morris et al., 1990), this pool needs to be replenished by PI from intracellular stores. It has been proposed that the PI-transfer protein may be involved in the intracellular transport of PI to the plasma membrane (Van Paridon et al., 1987a).
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Wirtz, K.W.A., Gadella, T.W.J., Verbist, J., Somerharju, P.J., Visser, A.J.W.G. (1991). Fluorescent Analogues of Phosphoinositides in Studies on Lipid-Protein Interactions and Membrane Dynamics. In: Gomez-Fernandez, J.C., Chapman, D., Packer, L. (eds) Progress in Membrane Biotechnology. ALS Advances in Life Sciences. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7454-0_5
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