G alpha(16) protein expression is up- and down-regulated following T-cell activation: Disruption of this regulation impairs activation-induced cell responses

被引:18
作者
Lippert, E
Baltensperger, K
Jacques, Y
Hermouet, S
机构
[1] INST BIOL, GRP RECEPTEURS & CYTOKINES, INSERM U463, F-44035 NANTES, FRANCE
[2] UNIV BERN, INST PHARMAKOL, BERN, SWITZERLAND
来源
FEBS LETTERS | 1997年 / 417卷 / 03期
基金
澳大利亚研究理事会;
关键词
G protein; G alpha(16); TCR activation; human T-lymphocyte;
D O I
10.1016/S0014-5793(97)01308-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 G alpha(16), the 43 kDa alpha subunit of G(16), varies widely, depending on T-cell activation status, Quiescent blood lymphocytes strongly up-regulate G alpha(16) after Leuco A stimulation: protein expression of G alpha(16) is maximal at day 4, then decreases, Consistently, in human T-cen clones, expression of G alpha(16), is high in the first week following activation and decreases rapidly within the second week. In addition, permanent disruption of regulated G alpha(16) expression in Jurkat T-cells by stable overexpression of 43 kDa G alpha(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 G alpha(16) expression is necessary far optimal activation-induced T-cell responses, and that G alpha(16) proteins may be involved in the negative regulation of TCR signalling. (C) 1997 Federation of European Biochemical Societies.
引用
收藏
页码:292 / 296
页数:5
相关论文
共 26 条
[1]   G-ALPHA-16, A G-PROTEIN ALPHA SUBUNIT SPECIFICALLY EXPRESSED IN HEMATOPOIETIC-CELLS [J].
AMATRUDA, TT ;
STEELE, DA ;
SLEPAK, VZ ;
SIMON, MI .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (13) :5587-5591
[2]  
Baltensperger H, 1997, J BIOL CHEM, V272, P10151
[3]  
BOURNE HR, 1991, NATURE, V349, P117, DOI 10.1038/349117a0
[4]   DISSECTION OF THYMOCYTE SIGNALING PATHWAYS BY INVIVO EXPRESSION OF PERTUSSIS TOXIN ADP-RIBOSYLTRANSFERASE [J].
CHAFFIN, KE ;
BEALS, CR ;
WILKIE, TM ;
FORBUSH, KA ;
SIMON, MI ;
PERLMUTTER, RM .
EMBO JOURNAL, 1990, 9 (12) :3821-3829
[5]   A PERTUSSIS TOXIN-SENSITIVE PROCESS-CONTROLS THYMOCYTE EMIGRATION [J].
CHAFFIN, KE ;
PERLMUTTER, RM .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1991, 21 (10) :2565-2573
[6]  
DAVODEAU F, 1993, J IMMUNOL, V151, P1214
[7]   AUTOCRINE T-CELL SUICIDE MEDIATED BY APO-1/(FAS/CD95) [J].
DHEIN, J ;
WALCZAK, H ;
BAUMLER, C ;
DEBATIN, KM ;
KRAMMER, PH .
NATURE, 1995, 373 (6513) :438-441
[8]   HLA-target antigens and T-cell receptor diversity of activated T cells invading the skin during acute graft-versus-host disease [J].
Gaschet, J ;
Trevino, MA ;
Cherel, M ;
Vivien, R ;
GarciaSahuquillo, A ;
Hallet, MM ;
Bonneville, M ;
Harrousseau, JL ;
Bragado, R ;
Milpied, N ;
Vie, H .
BLOOD, 1996, 87 (06) :2345-2353
[9]  
GOLDSMITH P, 1987, J BIOL CHEM, V262, P14683
[10]   Differential G-protein expression during B- and T-cell development [J].
Grant, KR ;
Harnett, W ;
Milligan, G ;
Harnett, MM .
IMMUNOLOGY, 1997, 90 (04) :564-571