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Although all three Vav family members are expressed in T lymphocytes, the role that Vav3 plays in T cell activation is poorly defined. Here we show that, like Vav1, Vav3 undergoes rapid tyrosine phosphorylation after T cell receptor (TCR) cross-linkage and interacts with the adaptor molecules SLP76 and 3BP2 in a SH2-dependent manner. However, depletion of Vav1 but not Vav3 protein by RNA interference affects TCR-mediated IL-2 promoter activity. In contrast, Vav3 function is specifically required for coupling TCR stimulation to serum response element-mediated gene transcription. These data indicate that, although both Vav proteins are biochemically coupled to the TCR, they regulate distinct molecular pathways leading to defined gene transcriptional events.

Original publication

DOI

10.1084/jem.20031228

Type

Journal article

Journal

J Exp Med

Publication Date

02/02/2004

Volume

199

Pages

429 - 434

Keywords

Cell Cycle Proteins, Gene Expression Regulation, Guanine Nucleotide Exchange Factors, Humans, Jurkat Cells, Oncogene Proteins, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-vav, Receptors, Antigen, T-Cell, T-Lymphocytes, Transcription, Genetic