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Blood, 15 April 2004, Vol. 103, No. 8, pp. 2997-3004. Prepublished online as a Blood First Edition Paper on January 8, 2004; DOI 10.1182/blood-2003-08-2768. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2768v1 103/8/2997    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Okamura, A. Articles by Matsui, T. Search for Related Content PubMed PubMed Citation Articles by Okamura, A. Articles by Matsui, T. Related Collections Hematopoiesis and Stem Cells Neoplasia Phagocytes Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Involvement of casein kinase I in cytokine-induced granulocytic differentiation Atsuo Okamura, Nobuko Iwata, Aki Nagata, Akira Tamekane, Manabu Shimoyama, Hiroshi Gomyo, Kimikazu Yakushijin, Norinaga Urahama, Miyuki Hamaguchi, Chie Fukui, Kazuo Chihara, Mitsuhiro Ito, and Toshimitsu Matsui From Hematology/Oncology, Department of Medicine, Kobe University School of Medicine, Kobe, Japan. Two closely related casein kinase I (CKI) isoforms, CKI and CKI, are ubiquitously expressed in many human tissues, but their specific biologic function remains to be clarified. Here, we provide the first evidence that CKI is involved in hematopoietic cell differentiation. CKI, but not CKI, was down-regulated along with human granulocytic differentiation. The specific down-regulation was observed in granulocyte colony-stimulating factor (G-CSF)–induced cell differentiation of murine interleukin-3 (IL-3)–dependent myeloid progenitor 32D cells. Introduction of wild-type (WT)–CKI into 32D cells inhibited the G-CSF–induced cell differentiation, whereas kinase-negative (KN)–CKI promoted the differentiation. Neither WT- nor KN-CKI affected IL-3–dependent cell growth. Moreover, introduction of WT- or KN-CKI did not affect the cytokine-induced cell growth and differentiation. While G-CSF–induced activation of signal transducers and activators of transcription 3 (STAT3) was sustained by KN-CKI, STAT3 activation was attenuated by WT-CKI. This may be explained by the fact that the suppressor of cytokine signaling 3 (SOCS3) was stabilized by its physical association with CKI. Such stabilization by CKI was also seen in IL-3–induced -catenin. The stabilization of downstream components of cytokine and Wnt signaling by CKI might be critical for integration of several intracellular signaling pathways to a cell-specific biologic response in hematopoietic cell self-renewal. (Blood. 2004;103: 2997-3004) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: A casein kinase making its case in granulopoiesis Ivo P. Touw Blood 2004 103: 2866-2867. [Full Text] [PDF]

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