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Receptor-Mediated Degradation of Choline Plasmalogens and Glycerophospholipid Methylation: A New Hypothesis

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Enzymes of Lipid Metabolism II

Part of the book series: NATO ASI Series ((NSSA,volume 116))

Abstract

The stimulation of receptors on the cell surface initiates biochemical and physical changes in membranes that lead to biological responses by the cells. The biochemical and physical changes include changes in levels of cyclic nucleotides, phosphorylation of proteins in membranes, increased membrane disorder (fluidity), and increased fluxes of Ca2+, Na+, and other ions. Changes in lipid metabolism associated with receptor stimulation may include the release of arachidonic acid and formation of metabolites and changes in phospholipid N-methylation and in polyphosphoinositide metabolism. The large number of studies on the association of phospholipid N-methylation with receptor stimulation and adenylate cyclase suggest that an important biological mechanism is involved. An overall hypothesis linking receptor stimulation directly with increased activity of AdoMet: PtdEtn methyltransferase and phospholipase A2 was proposed (Hirata and Axelrod, 1980; Mato and Alemany, 1983). This hypothesis is no longer tenable because of difficulties of others with reproduction of the results, problems inherent in the methodology, and errors in the interpretation of the results. Most previous studies failed to recognize that stopping a reaction with acid causes the hydrolysis of plasmalogens to lysoGpl. The presence of lyso compounds was instead interpreted as evidence for phospholipase A2 activity.

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Abbreviations

Gpl:

glycerophospholipids

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© 1986 Plenum Press, New York

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Horrocks, L.A. et al. (1986). Receptor-Mediated Degradation of Choline Plasmalogens and Glycerophospholipid Methylation: A New Hypothesis. In: Freysz, L., Dreyfus, H., Massarelli, R., Gatt, S. (eds) Enzymes of Lipid Metabolism II. NATO ASI Series, vol 116. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5212-9_85

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  • DOI: https://doi.org/10.1007/978-1-4684-5212-9_85

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5214-3

  • Online ISBN: 978-1-4684-5212-9

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