Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 199, Issue 3, Pages 369-379Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20030589
Keywords
signal transduction; Src kinases; SH3 domain; T cell antigen receptor; IL-2
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Funding
- NIAID NIH HHS [AI46004, AI50179, R01 AI050179] Funding Source: Medline
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The first step in T cell receptor for antigen (TCK) signaling is the activation of the receptor-bound Src kinases, Lck and Fyn. The exact mechanism of this process is unknown. Here, we report that the novel Src homology (SH) 3/SH2 ligand-Uncoordinated 119 (Unc119) associates with CD3 and CD4, and activates Lck and Fyn. Unc119 overexpression increases Lck/Fyn activity in T cells. In Unc119-deficient T cells, Lck/Fyn activity is dramatically reduced with concomitant decrease in interleukin 2 production and cellular proliferation. Reconstitution of cells with Unc119 reverses the signaling and functional outcome. Thus, Unc119 is a receptor-associated activator of Src-type kinases. It provides a novel mechanism of signal generation in the TCR complex.
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