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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.
Submitted August 12, 2003
Accepted December 27, 2003
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*
Hematology/Oncology, Department of Medicine, Kobe University School of Medicine, Kobe, Hyogo, Japan
* Corresponding author; email: matsui{at}med.kobe-u.ac.jp.
Two closely related casein kinase I (CKI)  and  are ubiquitously expressed in many human tissues, but their specific biological 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) were sustained by KN-CKI, it 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 signalings by CKI might be critical for integration of several intracellular signalings to a cell-specific biological response in the hematopoietic cell self-renewal.
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