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Blood, 15 April 2007, Vol. 109, No. 8, pp. 3360-3368. Prepublished online as a Blood First Edition Paper on December 7, 2006; DOI 10.1182/blood-2006-07-033662. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-07-033662v1 109/8/3360    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 Miletic, A. V. Articles by Swat, W. Search for Related Content PubMed PubMed Citation Articles by Miletic, A. V. Articles by Swat, W. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 5, 2006 Accepted November 30, 2006 Vav proteins control MyD88-dependent oxidative burst Ana V. Miletic, Daniel B. Graham, Vivianne Montgrain, Keiko Fujikawa, Tracie Kloeppel, Karry Brim, Brian Weaver, Robert Schreiber, Ramnik Xavier, and Wojciech Swat* Dept of Pathology & Immunology, Washington University School of Medicine & Siteman Cancer Center, St. Louis, MO, United States Dept of Biochemistry, Hokkaido University School of Medicine, Sapporo, Japan Dept of Medicine, Massachussetts General Hospital, Boston, MA, United States * Corresponding author; email: swat{at}wustl.edu. The importance of reactive oxygen intermediate (ROI) production in antimicrobial responses is demonstrated in human patients who suffer from chronic granulomatous disease (CGD) due to defective NADPH oxidase function. Exactly how bacterial products activating Toll-like receptors (TLRs) induce oxidative burst is unknown. Here, we identify the Vav family of Rho GEFs as critical mediators of LPS-induced MyD88-dependent activation of Rac2, NADPH oxidase, and ROI production, using mice deficient in Vav1, Vav2, and Vav3. Vav proteins are also required for p38 MAP kinase activation and for normal regulation of proinflammatory cytokine production, but not for other MyD88-controlled effector pathways such as those involving JNK, COX2 or iNOS and the production of reactive nitrogen intermediates (RNI). Thus, our data indicate that Vav specifically transduces a subset of signals emanating from MyD88. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: O. Shibolet, C. Giallourakis, I. Rosenberg, T. Mueller, R. J. Xavier, and D. K. Podolsky AKAP13, a RhoA GTPase-specific Guanine Exchange Factor, Is a Novel Regulator of TLR2 Signaling J. Biol. Chem., November 30, 2007; 282(48): 35308 - 35317. [Abstract] [Full Text] [PDF] A. C. Azim, H. Cao, X. Gao, M. Joo, A. B. Malik, R. B. van Breemen, R. T. Sadikot, G. Park, and J. W. Christman Regulation of cyclooxygenase-2 expression by small GTPase Rac2 in bone marrow macrophages Am J Physiol Lung Cell Mol Physiol, September 1, 2007; 293(3): L668 - L673. [Abstract] [Full Text] [PDF]

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