Premium
SOCS‐1 can suppress CD3ζ‐ and Syk‐mediated NF‐AT activation in a non‐lymphoid cell line
Author(s) -
Matsuda Tadashi,
Yamamoto Tetsuya,
Kishi Hiroyuki,
Yoshimura Akihiko,
Muraguchi Atsushi
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01444-7
Subject(s) - syk , microbiology and biotechnology , t cell receptor , jurkat cells , signal transduction , t cell , cd3 , cd8 , cytokine , tyrosine kinase , chemistry , cancer research , biology , immune system , immunology
To elucidate T cell antigen receptor (TCR) signaling leading to activation nuclear factor of activated T cells (NF‐AT), we reconstituted TCR signaling to activate NF‐AT in a non‐lymphoid cell line, 293T. We demonstrated that co‐expression of CD8/ζ and Syk were necessary for NF‐AT activation in 293T. This NF‐AT response was completely inhibited by the addition of cyclosporin A or FK506, but markedly enhanced by the additional expression of Tec protein tyrosine kinase. We also show that the cytokine signaling suppressor, suppressor of cytokine signaling 1, potently inhibited this response by interacting with Syk and immunoreceptor tyrosine‐based activation motifs in CD8/ζ. These results imply that this novel system may provide a useful tool to delineate or identify the regulatory molecules for CD3ζ/Syk‐mediated NF‐AT activation.