Biosynthesis, Storage and Mobilization of Arachidonic Acid

A basic principle that has emerged from the last decade of research on lipid signaling is that membrane phospholipids should be regarded not only as structural components of the cell, but also as precursors for transmembrane, or even transcellular, signaling molecules. In Table 2.1, I have listed a series of examples to illustrate this principle. Three components play a major role in 

Precursor phospholipase signaling molecule(s) biological effectors 

PC phospholipase C 1,2 diacylglycerol inositol-trisphosphate protein kinase C intracellular [Ca2+] 

PC phospholipase D phosphatidic acid phosphatidic acid-dependent protein kinase 

PE phospholipase A2 arachidonate protein kinases, ion channels, further metabolism 

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Calcium ionophores, such as A23187 and X538A, are known to stimulate thromboxane biosynthesis in platelets [168]. These compounds mobilize calcium from intracellular storage sites, leading to an increased calcium concentration in the cytosol. This in turn stimulates the release of arachidonic acid from its esterified storage form, and the subsequent conversion into prostaglandins and thromboxanes is thus increased [168]. 

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