Inhibition of protein synthesis by the T cell receptor-inducible human TDAG51 gene product.

The T cell death associated gene 51 (TDAG51) was shown to be required for T cell receptor (TCR)-dependent induction of Fas/Apo1/CD95 expression in a murine T cell hybridoma. Despite the absence of a nuclear localization sequence and a nucleic acid binding domain, it was suggested to be localized in the ...
nucleus and to function as a transcription factor regulating Fas-expression. However, we demonstrate that the human (h)TDAG51 protein is localized in the cytoplasm and the nucleoli, suggesting a role in ribosome biogenesis and/or translation regulation. Indeed, it strongly inhibited translation of a luciferase mRNA in a reticulocyte translational extract. Furthermore, cotransfection of hTDAG51 and the luciferase gene into 293T cells resulted in a strong inhibition of luciferase mRNA translation. Our findings were further strengthened by isolating in a yeast two-hybrid screen three proteins which are involved in the regulation of translation. We speculate that hTDAG51 couples TCR signaling to inhibition of protein biosynthesis in activated T lymphocytes.
Mesh Terms:
Animals, Apoptosis, B-Lymphocytes, Cell Line, Transformed, Cell Nucleolus, Gene Expression, Humans, Hybridomas, Luciferases, Mammals, Peptide Initiation Factors, Poly(A)-Binding Proteins, Prokaryotic Initiation Factor-3, Protein Biosynthesis, RNA, Messenger, RNA-Binding Proteins, Receptors, Antigen, T-Cell, Ribosomal Proteins, Signal Transduction, T-Lymphocytes, Transcription Factors, Two-Hybrid System Techniques, Yeasts
Cell. Signal.
Date: May. 01, 2001
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