AKT1/PKBα is recruited to lipid rafts and activated downstream of PKC isotypes in CD3‐induced T cell signaling

FEBS Letters

Jenny, Marcel²  Bauer, Birgit¹  Fresser, Fiedrich¹  Überall, Florian²  Baier, Gottfried¹ 

[1] Department of Medical Biology and Human Genetics, University of Innsbruck, Schöpfstr. 41, A-6020 Innsbruck, Austria;Department of Medical Chemistry and Biochemistry, University of Innsbruck, Schöpfstr. 41, A-6020 Innsbruck, Austria

关键词: T cell;    T cell receptor signaling;    Raft;    Protein kinase Cθ;    Akt-1;    Nuclear factor κB;    CTB;    cholera toxin B;    NF-κB;    nuclear factor κB;    PMA;    phorbol myristate acetate;    PH;    pleckstrin homology;    PI-3K;    phosphatidylinositol 3-kinase;    PIP3;    phosphatidylinositol 3;    4;    5-trisphosphate;    PKA;    protein kinase A;    PKB;    protein kinase B;    PKC;    protein kinase C;    cPKC and nPKC;    conventional and novel PKC subfamilies;    respectively;    TCR;    T cell receptor;   

DOI  :  10.1016/S0014-5793(03)00287-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Protein kinase (PK) Cθ and Akt/PKBα cooperate in T cell receptor/CD28-induced T cell signaling. We here demonstrate the recruitment of endogenous Akt1 and PKCθ to lipid rafts in CD3-stimulated T cells. Further we show that Myr-PKCθ mediates translocation of endogenous Akt1 to the plasma membrane as well as to lipid rafts, most likely explained by the observed complex formation of both protein kinases. In addition, in peripheral mouse T cells, the PKC inhibitor Gö6850 could partially block Akt1 activation in CD3-induced signaling, placing PKC isotype(s) upstream of Akt1. However, T cells derived from PKCθ knockout mice were not impaired in CD3- or phorbol ester-induced Akt1 activity. Taken together, the results of this study give new insights into the functional link of Akt1 and PKCθ in T cell signaling, demonstrating the co-recruitment of the two kinases and showing a novel pathway leading to Akt1 transactivation where PKC isotype(s) are involved but PKCθ is not essential.

【 授权许可】

Unknown