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Cardiovascular Research 2003 60(2):215-216; doi:10.1016/j.cardiores.2003.09.005
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

PAF, PIP3 and NO: emerging role in reperfusion injury

Axel Gödecke*

Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität, Universitätsstr.1, 40225 Düsseldorf, Germany

*Tel.: +49-211-8112675; fax: +49-211-8112675. Email address: Axel.Goedecke@uni-duesseldorf.de

Received 3 September 2003;
The first 10% of the full text of this article appears below.

Phosphatidylinositol 3-kinases (PI3Ks) constitute a ubiquitously expressed family of lipid kinases that phosphorylate the membrane lipid phosphatidylinositol 4,5-bisphosphate on position D3 of the inositol moiety, leading to formation of the second messenger phosphatidylinositol 3,4,5-trisphosphate (PIP3) [1]. PI3Ks are heterodimeric enzymes that are composed of a catalytic and a regulatory subunit. PI3K{alpha}, -β, and -{delta} (class Ia enzymes) respond to activated receptor tyrosine kinases like the insulin and PDGF receptors either by direct interaction of the regulatory subunit with phosphorylated receptor tyrosine residues or via adaptor molecules. In contrast, PI3K{gamma} (the only member of the class Ib family) is activated by β{gamma} subunits of heterotrimeric G proteins in response to stimulation of heptahelical G-protein-coupled receptors (GPCRs). In addition, activated RAS may . . . [Full Text of this Article]


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