The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published 2 February 2004. doi:10.1084/jem.20031228
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 3, 429-434
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Brief Definitive Report

 Differential Regulation of TCR-mediated Gene Transcription by Vav Family Members

Shaheen Zakaria1, Timothy S. Gomez2, Doris N. Savoy1, Simon McAdam3, Martin Turner3, Robert T. Abraham4, and Daniel D. Billadeau1,2

1 Division of Developmental Oncology Research, Mayo Clinic College of Medicine, Rochester, MN 55905
2 Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905
3 Lymphocyte Signaling and Development Laboratory, Molecular Immunology Programme, Babraham Institute, Babraham, Cambridge CB2 4AT, UK
4 The Burnham Institute, La Jolla, CA 92037

Address correspondence to Daniel D. Billadeau, Div. of Oncology Research, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. Phone: (507) 266-4334; Fax: (507) 266-5146; email: billadeau.daniel{at}mayo.edu

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.

Key Words: T cell • signal transduction • Vav • GEF • SRE


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