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Prepublished online as a Blood First Edition Paper on June 21, 2002; DOI 10.1182/blood-2002-04-1149. This Article Full Text (PDF) All Versions of this Article: 2002-04-1149v1 100/8/2692    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bokoch, G. M Articles by Diebold, B. A Search for Related Content PubMed PubMed Citation Articles by Bokoch, G. M Articles by Diebold, B. A Social Bookmarking                   What's this? Submitted April 16, 2002 Accepted June 4, 2002 Current molecular models for NADPH oxidase regulation by Rac GTPase Gary M Bokoch* and Becky A Diebold Department of Immunology, The Scripps Research Institute, La Jolla, CA, USA * Corresponding author; email: bokoch{at}scripps.edu. Reactive oxygen species (ROS) have been increasingly recognized as important components of cell signaling, in addition to their well-established roles in host defense. The formation of ROS in phagocytic- and nonphagocytic cells involves membrane-localized and Rac GTPase-regulated NADPH oxidase(s). We discuss here the current molecular models for Rac GTPase action in the control of the phagocytic leukocyte NADPH oxidase. As a mechanistically detailed example of Rac GTPase signaling, the NADPH oxidase provides a potential paradigm for signaling by Rho family GTPases in general. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. 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