Abstract

The phospholipid base-exchange reactions catalyze the calcium dependent, non-energy requiring incorporation of serine, ethanolamine and choline into phosphatidylserine (PS), phosphatidylethanolamine (PE) and phosphatidylcholine (PC), respectively (Porcellati et al., 1971; Kanfer, 1972). This may be the only pathway for the de novo synthesis of PS in mammalian cells, whereas different pathways exist for the synthesis of PC and PE. PS can be translocated to the mitochondria where it is decarboxylated to form PE (Butler and Morell, 1983). Moreover, progressive methylation of PE leads to PC synthesis at the endoplasmic reticulum level. Thus, base-exchange reactions, together with decarboxylation of PS and subsequent methylation of PE to form PC may play a key role in both the net synthesis of PS and the remodeling of pre-existing phospholipids (Bjerve, 1985; Voelker, 1990; Vance, 1991). Experimental evidence suggests that base-exchange reactions are regulated by phosphorylation-dephosphorylation processes (Kanfer et al., 1988), long chain bases such as oleoylamine and sphingosine (Singh et al., 1992), unsaturated fatty acids (Kanfer and McCartney, 1991) and phospholipids (Corazzi et al., 1991). The three base-exchange activities are present in rat brain synaptosomal plasma membranes (Holbrook and Wurtman, 1988) and plasma membranes isolated from rat liver (Siddiqui and Exton, 1992). Recently, it has been shown that phospholipid base-exchange activity can be regulated upon G-protein and receptor activation (Siddiqui and Exton, 1992). These findings indicate that base-exchange activities may play a role in signal transduction-related events.

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