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We show here that Vav-2 is tyrosine phosphorylated following antigen receptor engagement in both B- and T-cells, but potentiates nuclear factor of activated T cells (NFAT)-dependent transcription only in B cells. Vav-2 function requires the N-terminus, as well as functional Dbl homology and SH2 domains. More over, the enhancement of NFAT-dependent transcription by Vav-2 can be inhibited by a number of dominant-negative GTPases. The ability of Vav-2 to potentiate NFAT-dependent transcription correlates with its ability to promote a sustained calcium flux. Thus, Vav-2 augments the calcium signal in B cells but not T cells, and a truncated form of Vav-2 can neither activate NFAT nor augment calcium signaling. The CD19 co-receptor physically interacts with Vav-2 and synergistically enhances Vav-2 phosphorylation induced by the B-cell receptor (BCR). In addition, we found that Vav-2 augments CD19-stimulated NFAT- dependent transcription, as well as transcription from the CD5 enhancer. These data suggest a role for Vav-2 in transducing BCR signals to the transcription factor NFAT and implicate Vav-2 in the integration of BCR and CD19 signaling.

Original publication




Journal article



Publication Date





6173 - 6184


Animals, Antigens, CD19, B-Lymphocytes, CD5 Antigens, Cells, Cultured, DNA-Binding Proteins, Humans, Jurkat Cells, Mice, NFATC Transcription Factors, Nuclear Proteins, Oncogene Proteins, Phosphorylation, Proto-Oncogene Proteins c-vav, Receptor Protein-Tyrosine Kinases, Receptors, Antigen, B-Cell, Signal Transduction, T-Lymphocytes, Transcription Factors, Transcription, Genetic, Tyrosine