Inositol phospholipid turnover in PAF transmembrane signalling.
In a variety of cells and tissues, platelet activating factor (PAF) stimulates phospholipase C catalyzed breakdown of phosphoinositides. This results in the generation of the second messengers, inositol trisphosphate and diglyceride. This process occurs independently of extracellular Ca2+. A number of PAF structural analogues, receptor antagonists and drugs have been utilized to pharmacologically probe the activation of phospholipase C. PAF stimulation of the phosphoinositide turnover was shown to be sensitive to pertussis toxin in some systems, but not in others. The involvement of guanine nucleotide binding protein(s) and tyrosine kinase(s) in this process have also been postulated. These developments give new insights into PAF-receptor function at the molecular level, and also provide leads towards a better understanding of the cellular responses to PAF.
Shukla
S D
SD
Department of Pharmacology, School of Medicine, University of Missouri, Columbia 65212.
D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D010716:Phosphatidylinositols / Q000378:metabolism*; D010972:Platelet Activating Factor / Q000502:physiology*; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface / Q000502:physiology; D043562:Receptors, G-Protein-Coupled; D015398:Signal Transduction; D010738:Type C Phospholipases / Q000378:metabolism
D010716:Phosphatidylinositols; D010972:Platelet Activating Factor; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D010738:Type C Phospholipases