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Submitted on October 24, 2007
Accepted on December 26, 2007
From the Laboratory of Pathology (J.S.I, D.D.R.), National Cancer Institute, National Institutes of Health, Bethesda, Md; and the Department of Biochemistry and Molecular Biophysics (W.A.F.), Washington University School of Medicine, St. Louis, Mo.
* To whom correspondence should be addressed. E-mail: frazier{at}wustl.edu.
Abstract—CD47, originally named integrin-associated protein, is a receptor for thrombospondin-1. A number of important roles for CD47 have been defined in regulating the migration, proliferation, and survival of vascular cells, and in regulation of innate and adaptive immunity. The recent discovery that thrombospondin-1 acts via CD47 to inhibit nitric oxide signaling throughout the vascular system has given new importance and perhaps a unifying mechanism of action to these enigmatic proteins. Here we trace the development of this exciting new paradigm for CD47 function in vascular physiology.
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