Differential activation of MAP kinase family members triggered by CD99 engagement

[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⁺.

[学科分类] 生物化学/生物物理

[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