Activation of JNK Signaling Pathway by Erythropoietin, Thrombopoietin, and Interleukin-3

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  • Yuka Nagata
    From the Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan; and the Department of Genetics and Molecular Biology, Institute for Virus Research, Kyoto University, Kyoto, Japan
  • Eisuke Nishida
    From the Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan; and the Department of Genetics and Molecular Biology, Institute for Virus Research, Kyoto University, Kyoto, Japan
  • Kazuo Todokoro
    From the Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan; and the Department of Genetics and Molecular Biology, Institute for Virus Research, Kyoto University, Kyoto, Japan

書誌事項

公開日
1997-04-15
DOI
  • 10.1182/blood.v89.8.2664
公開者
American Society of Hematology

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説明

<jats:title>Abstract</jats:title><jats:p>A variety of environmental stresses, such as osmotic shock, UV radiation, and heat shock, or the proinflammatory cytokines tumor necrosis factor-α and interleukin-1 reportedly induce activation of c-Jun amino-terminal kinases (JNK), which are usually activated by SEK1/MKK4. We report here that the hematopoietic cytokines interleukin-3 (IL-3), erythropoietin (Epo), and thrombopoietin (Tpo), which regulate growth and differentiation of hematopoietic progenitor cells, erythroids, and megakaryocytes/platelets, respectively, also activate a JNK signaling cascade. In-gel kinase assay as well as in vitro kinase assay clearly showed that IL-3, Epo, and Tpo rapidly and transiently activated both JNK1 and JNK2 in IL-3–, Epo-, or Tpo-dependent mouse hematopoietic progenitor cells. However, immunoblot analysis and in vitro kinase assay showed that neither phosphorylation nor activation of SEK1/MKK4 was induced by IL-3, Epo, or Tpo stimulation. Therefore, we concluded that the JNK signaling cascade plays an important role not only in stress responses and proinflammatory cytokine actions but also in hematopoietic cytokine actions and that hematopoietic cytokines may activate the JNKs through a kinase other than SEK1/MKK4, as previously suggested for stress-activated cells.</jats:p>

収録刊行物

  • Blood

    Blood 89 (8), 2664-2669, 1997-04-15

    American Society of Hematology

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