Differential activation of MAP kinase family members triggered by CD99 engagement

FEBS Letters

Kim, Tae Jin¹  Song, Hyung Geun²  Hahn, Myong-Joon⁴  Yoon, Sang Soon¹  Sohn, Hae Won³  Park, Seong Hoe³ 

[1] Department of Pathology, Sungkyunkwan University School of Medicine, Suwon 440-746, South Korea;Department of Pathology, Chungbuk National University College of Medicine, Cheongju 361-763, South Korea;Department of Pathology, Seoul National University College of Medicine, Seoul 110-799, South Korea;Department of Microbiology, Sungkyunkwan University School of Medicine, Suwon 440-746, South Korea

关键词: T lymphocyte;    Cellular activation;    Signal transduction;    Cell surface molecule;    Protein kinase/phosphatase;    MAPK;    mitogen-activated protein kinase;    PI-3K;    phosphatidylinositol-3 kinase;    JNK;    c-jun N-terminal kinase;    ERK;    extracellular signal-regulated kinase;    PKC;    protein kinase C;    MEK;    MAPK kinase;    BAPTA-AM;    1;    2-bis(o-aminophenoxy)ethane-N;    N;    N′;    N′-tetraacetic acid tetra(acetoxymethyl) ester;    mAb;    monoclonal antibody;   

DOI  :  10.1016/S0014-5793(00)01330-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The molecular basis for the modulatory properties of CD99 is not well understood. Treatment of human Jurkat T lymphocytes with anti-CD99 antibody led to activation of three mitogen-activated protein kinase (MAPK) members, ERK, JNK, and p38 MAPK, along with homotypic aggregation. While phosphorylation of ERK and JNK was inhibited by the pretreatment of a PKC inhibitor, bisindolylmaleimide I, activation of p38 MAPK was upregulated by the same pretreatment. The signaling pathways to MAPKs by CD99 engagement were independent of PI-3 kinase, distinguishing from those by CD3 engagement. Among MAPKs, ERK pathway was essential for homotypic aggregation together with intracytoplasmic Ca²⁺.

【 授权许可】

Unknown