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Gα 16 protein expression is up‐ and down‐regulated following T‐cell activation: disruption of this regulation impairs activation‐induced cell responses
Author(s) -
Lippert Eric,
Baltensperger Kurt,
Jacques Yannick,
Hermouet Sylvie
Publication year - 1997
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(97)01308-2
Subject(s) - heterotrimeric g protein , jurkat cells , microbiology and biotechnology , t cell , cell , g protein , apoptosis , biology , signal transduction , chemistry , immune system , biochemistry , immunology
The role of heterotrimeric G proteins in T‐cell activation is poorly understood. Here we show that in normal, mature human T‐cells, expression of Gα 16 , the 43 kDa α subunit of G 16 , varies widely, depending on T‐cell activation status. Quiescent blood lymphocytes strongly up‐regulate Gα 16 after Leuco A stimulation: protein expression of Gα 16 is maximal at day 4, then decreases. Consistently, in human T‐cell clones, expression of Gα 16 is high in the first week following activation and decreases rapidly within the second week. In addition, permanent disruption of regulated Gα 16 expression in Jurkat T‐cells by stable overexpression of 43 kDa Gα 16 inhibited Leuco A‐induced interleukin‐2 production, CD69 up‐regulation and cell apoptosis (by 58%, 46% and 74%, respectively), suggesting that coordinate regulation of Gα 16 expression is necessary for optimal activation‐induced T‐cell responses, and that Gα 16 proteins may be involved in the negative regulation of TCR signalling.