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Blood, 1 April 2004, Vol. 103, No. 7, pp. 2443-2451. Prepublished online as a Blood First Edition Paper on October 30, 2003; DOI 10.1182/blood-2003-08-2834. This Article Full Text (PDF) All Versions of this Article: 2003-08-2834v1 103/7/2443    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 Katzav, S. Search for Related Content PubMed PubMed Citation Articles by Katzav, S. Social Bookmarking                   What's this? Submitted August 26, 2003 Accepted October 16, 2003 Vav1 - an oncogene that regulates specific transcriptional activation of T cells Shulamit Katzav* Hubert H. Humphrey Center for Experimental Medicine & Cancer Research, The Hebrew University/Hadassah Medical School, Jerusalem, Israel * Corresponding author; email: katzav{at}cc.huji.ac.il. The nuclear factor of activated T cells (NFAT) proteins are a family of transcription factors whose activation is controlled by calcineurin, a Ca2-dependent phosphatase. Once dephosphorylated, these proteins move to the nucleus where they interact with co-factors to form transcription factor complexes. Inhibition of NFAT proteins by immunosuppressants such as cyclosporin A (CsA) and FK506, is used clinically to prevent transplant rejection. Although these drugs have revolutionized organ transplant, their use is associated with severe side effects in other organs in which NFAT proteins are important. One of the signal transducers that controls NFAT activity is Vav1, which is exclusively expressed in the hematopoietic system. Vav1 contains numerous modular domains that enable its function as a guanine exchange factor (GEF) towards RhoGTPases, as well as participate in protein-protein interactions. This review focuses on the mechanisms by which Vav1 regulates NFAT through GEF dependent and independent cascades, emphasizing the newly assigned role of Vav1 in the regulation of Ca2 release. Because of its restriction to hematopoietic cell lineages and its importance in the regulation of NFAT, targeting Vav1 and, in particular, its association with other proteins, may offer a highly selective means of modifying T-cell behaviour, thus allowing the development of more specific immunosuppressive therapies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Schunke, P. Span, H. Ronneburg, A. Dittmer, M. Vetter, H.-J. Holzhausen, E. Kantelhardt, S. Krenkel, V. Muller, F. C.G.J. Sweep, et al. Cyclooxygenase-2 Is a Target Gene of Rho GDP Dissociation Inhibitor {beta} in Breast Cancer Cells Cancer Res., November 15, 2007; 67(22): 10694 - 10702. [Abstract] [Full Text] [PDF] A. D. Joshi, G. V. Hegde, J. D. Dickinson, A. K. Mittal, J. C. Lynch, J. D. Eudy, J. O. Armitage, P. J. Bierman, R. G. Bociek, M. P. Devetten, et al. ATM, CTLA4, MNDA, and HEM1 in High versus Low CD38 Expressing B-Cell Chronic Lymphocytic Leukemia Clin. Cancer Res., September 15, 2007; 13(18): 5295 - 5304. [Abstract] [Full Text] [PDF] Z. Zhou, J. Yin, Z. Dou, J. Tang, C. Zhang, and Y. Cao The Calponin Homology Domain of Vav1 Associates with Calmodulin and Is Prerequisite to T Cell Antigen Receptor-induced Calcium Release in Jurkat T Lymphocytes J. Biol. Chem., August 10, 2007; 282(32): 23737 - 23744. [Abstract] [Full Text] [PDF] Q. Chen, A. Coffey, S. G. Bourgoin, and M. Gadina Cytohesin Binder and Regulator Augments T Cell Receptor-induced Nuclear Factor of Activated T Cells{middle dot}AP-1 Activation through Regulation of the JNK Pathway J. Biol. Chem., July 21, 2006; 281(29): 19985 - 19994. [Abstract] [Full Text] [PDF]

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