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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.R800024-JLR200 on October 6, 2008

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Journal of Lipid Research, Vol. 50, S255-S259, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Signaling

The emerging roles of PAF acetylhydrolase

Thomas M. McIntyre1,*, Stephen M. Prescott{dagger} and Diana M. Stafforini§

* Department of Cell Biology, Lerner Research Institute, Cleveland Clinic College of Medicine of Case Western Reserve University, Cleveland, OH 44195
{dagger} Oklahoma Medical Research Foundation, Oklahoma City, OK 73104
§ Huntsman Cancer Institute and Department of Internal Medicine, University of Utah, Salt Lake City, UT 84112

This work was supported by National Institutes of Health Grants HL44513, HL35828, and HL087018.

Published, JLR Papers in Press, October 6, 2008.

1 To whom correspondence should be addressed. e-mail: mcintyt{at}ccf.org


ABSTRACT

Platelet-activating factor (PAF), a phospholipid autacoid with potent effects throughout the innate immune system, is selectively degraded by two small families of PAF acetylhydrolases (PAF-AHs). These Ca2+-independent phospholipases A2 display remarkable specificity for the length of the sn-2 residue, but this selectivity is lost as the residue gains oxygen functions. Two of the PAF-AHs therefore are specific oxidized phospholipid phospholipases that reduce inflammation, but also remove oxidatively truncated phospholipids that induce apoptosis. The roles of these enzymes are manifold, and their separate and combined functions are now being addressed in model systems and clinical studies

Supplementary key words oxidized phospholipids • Lp-PLA2 • platelet-activating factor


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JLR 50th Anniversary Collections
Anniversary Collection::Signaling



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