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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.R800067-JLR200 on November 24, 2008

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Journal of Lipid Research, Vol. 50, S358-S363, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology


Atherogenesis

A systems-based framework for understanding complex metabolic and cardiovascular disorders

Sulin Wu*, Aldons J. Lusis*,{dagger} and Thomas A. Drake1,§

* Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1679
{dagger} Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA 90095-1679
§ Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1679

Published, JLR Papers in Press, November 24, 2008.

1 To whom correspondence should be addressed. e-mail: TDrake{at}mednet.ucla.edu


ABSTRACT

Common forms of metabolic and cardiovascular diseases involve the interplay of numerous genes as well as important environmental factors. Traditional biochemical and genetic approaches generally attempt to dissect these diseases one gene at a time, for example, by analysis of Mendelian forms or genetically engineered experimental organisms. But, it is also important to understand how the genes interact with each other and the environment, and how these interactions change in disease states. Technological advances, such as the development of expression arrays that allow quantification of all transcript levels in a cell or tissue, have made it feasible to globally monitor molecular phenotypes that underlie disease states. By applying statistical methods, relationships between DNA variation, gene expression patterns, and diseases can be modeled.

Supplementary key words DNA variation • gene network • complex traits


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JLR 50th Anniversary Collections
Anniversary Collection::Atherogenesis




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Copyright © 2009 by the American Society for Biochemistry and Molecular Biology.
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