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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1106-1113.
Prepublished online as a Blood First Edition Paper on September 2, 2004; DOI 10.1182/blood-2003-08-2965.
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Submitted August 29, 2003
Accepted August 19, 2004
The adaptor protein 3BP2 associates VAV guanine nucleotide exchange factors to regulate NFAT activation by the B cell antigen receptor
Isabelle Foucault, Severine Le Bras, Celine Charvet, Cheol Moon, Amnon Altman, and Marcel Deckert*
Institut National de la Sante et de la Recherche Medicale Unite 576, Hopital de l'Archet, Nice, France
Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA, USA
* Corresponding author; email: deckert{at}unice.fr.
Engagement of B cell antigen receptor (BCR) activates kinases of the Src and Syk families and signaling complexes assembled by adaptor proteins, which dictate B cell fate and function. The adaptor 3BP2/SH3BP2, an Abl SH3-binding and Syk-kinases interacting protein, exhibits positive regulatory roles in T, NK and basophilic cells. However, its involvement in BCR signaling is completely unknown. Here we show that 3BP2 is tyrosine phosphorylated following BCR aggregation on B lymphoma cells, and that 3BP2 is a substrate for Syk and Fyn, but not Btk. To further explore the function of 3BP2 in B cells, we screened a yeast two-hybrid B lymphocyte library and found 3BP2 as a binding partner of Vav proteins. The interaction between 3BP2 and Vav proteins involved both constitutive and inducible mechanisms. 3BP2 also interacted with other components of BCR signaling pathway, including Syk and PLC- . Furthermore, overexpression and RNAi blocking experiments showed that 3BP2 regulated BCR-mediated nuclear factor of activated T cells (NFAT) activation. Finally, evidence was provided that 3BP2 functionally cooperates with Vav proteins and Rho GTPases to activate NFAT. Our results show that 3BP2 may regulate BCR-mediated gene activation through Vav proteins.
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