Inositol phosphatidyl

Phosphatidyl inositol may be degraded by one of two pathways. Dawson (1959) showed that an enzyme preparation from P. notatum breaks down phosphatidyl inositol by a series of reactions analogous to those catalysed by phospholipase A (Reaction 35) phospholipase B or lysophosphofipase (Reaction 36) GPC-diesterase (Reaction 39) and phosphomonoesterase (Reaction 40). Kemp, Hub-SCHER and Hawthorne (1961) reported a similar degradation of phosphatidyl inositol by a rat fiver enzyme preparation. The fiver enzyme does not attack lecithin or any of the other glycerophosphatides, whereas the P. notatum enzyme of Dawson (1959) hydrolyses lysolecithin. 

A second enzyme active towards phosphatidyl inositol is present in ox pancreas (Dawson 1959) and rat fiver (Kemp et al. 1961). With this enzyme the lipid is broken down into diglyceride and inositol monophosphate by a reaction analogous to the hydrolysis of lecithin by phospholipase C (Reaction 37). The enzjmae does not hydrolyse lecithin. 

Thus phosphatidyl inositol may be broken down by enzymes similar to the phosphohpases A, B and C that attack other glycerophosphatides, but apparently quite distinct from these enzymes. Kemp et al. (1961) suggested that the enzymes responsible for the degradation of phosphatidyl inositol be referred to as phospho-inositidases. Until these enzymes have been purified further and the possible effects of cationic and anionic amphipathic substances have been fully explored, such a suggestion would appear to be premature. 

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Pseudopterosin A is a member of a group of marine natural products which show potent antiinflammatory properties, but which are not prostaglandin biosynthesis inhibitors. Structurally similar to phosphatidyl inositol, they may function as phospholipase inhibitors, and, as such, may be the forerunners of a new class of therapeutic agents. 

Lassing, I Lindberg, U. (1988). Evidence that the phosphatidyl-inositol cycle is linked to cell motility. Expt. Cell Res. 174, 1-15. 

A. Inositol Phosphates.—Phosphatidyl inositol (71) is hydrolysed in mammalian tissues to wyo-inositol 1,2-cyclic phosphate (72).i myoinositol 1-phosphate (73) is released simultaneously but is not converted into (72) by the enzyme system. Periodate oxidation of (73) liberates orthophosphate quantitatively, the unstable dialdehyde phosphate (74) being an intermediate. Little or no orthophosphate is released from glucose 6-phosphate under the same oxidative conditions, and this reaction has been used to assay (73). 

Soya lecithin is a natural product which contains about 34% glycerides (soya oil), 5% sugars, and 61% phosphatides. The phosphatides in turn are comprised of phosphatidyl choline, i.e., chemical lecithin (20%), phosphatidyl ethanolamine (20%), and phosphatidyl inositol (21%). 

Groves, J. T., Wiilfing, C. and Boxer, S. G. (1996) Electrical manipulation of glycan-phosphatidyl inositol-tethered proteins in planar supported bilayers. Biophys.J., 71, 2716-2723. 

Desai, D.M., Newton, M.E., Kadlecek, T. and Weiss, A. (1990) Stimulation of the phosphatidyl-inositol pathway can induce T-cell activation. Nature 348, 66-69. 

Phosphatidyl Glycerol Phosphatidyl Inositol Cerebrosides Gangliosides... 

The other activity associated with transmembrane receptors is phospholipase C. Phosphatidyl inositol is a membrane phospholipid that after phosphorylation on the head group is found in the membrane as a phos-photidylinostitol bis phosphate. Phospholipase C cleaves this into a membrane associated diacylglycerol (the lipid part) and inositol trisphosphate (IP3, the soluble part). Both play a later role in elevating the level of the second messenger, Ca2+. 

HMIT is a H+-coupled myo-inositol symporter. High levels of its expression are observed in neurons and glia of hippocampus, hypothalamus, cerebellum and brainstem. Since myo-inositol is a precursor for phosphatidyl inositol, which itself is a critical regulator of many neuronal processes (Ch. 20), HMIT regulation is possibly involved in various mood and behavior patterns that are affected by inositol metabolism and by pharmacologic agents that modify inositol metabolism (see Chs 54 and 55). 

A similar study was conducted by Shoelson. Phosphatidyl inositol 3-kinase is activated by contact with autophosphorylated tyrosine kinase receptors followed by agonist binding to the cell-surface receptor. The truncated regulatory subunit of the enzyme (p85), which contains an SH2 domain, retained its full... 

Figure 7. Lipophilicity profile of propranolol in liposomes composed of zwitterionic and charged lipids (phosphatidyl ethanolamine (PE), oleic acid (OA), phosphatidyl inositol (PI)). Conditions of measurements are described in [113]. The dotted line indicates the partitioning profile of propranolol in the egg PC liposome system. The bars show the pH-dependent charge profile of propranolol (hatched bars positively charged propranolol) and the lipids in the membrane (black bars negatively charged lipids). Reprinted from [113] Kramer, S. (2001). Liposome/water partitioning , In Pharmacokinetic Optimization in Drug Research, eds. Testa, B. et al. Reproduced by permission of Verlag Helvetica Chimica Acta, Zurich...

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