FEBS letters · 2000
Differential activation of MAP kinase family members triggered by CD99 engagement.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Hahn M J, Yoon S S, Sohn H W, Song H G, Park S H, Kim T J
Аннотация
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 Ca(2+).
Предметные рубрики MeSH
Antibodies, MonoclonalCalciumCalcium-Calmodulin-Dependent Protein KinasesCell AdhesionChelating AgentsEgtazic AcidEnzyme ActivationHumansHyaluronan ReceptorsJNK Mitogen-Activated Protein KinasesJurkat CellsMAP Kinase Kinase 1MAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Kinase CProtein Serine-Threonine KinasesReceptor AggregationT-Lymphocytesp38 Mitogen-Activated Protein Kinases