[HTML][HTML] Differential activation of MAP kinase family members triggered by CD99 engagement
MJ Hahn, SS Yoon, HW Sohn, HG Song, SH Park… - FEBS letters, 2000 - Elsevier
MJ Hahn, SS Yoon, HW Sohn, HG Song, SH Park, TJ Kim
FEBS letters, 2000•ElsevierThe 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 …
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 …
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+.
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