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 Blood, 15 May 2004, Vol. 103, No. 10, pp. 3744-3750.
Prepublished online as a Blood First Edition Paper on February 5, 2004; DOI 10.1182/blood-2003-09-3126.

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HEMATOPOIESIS

Pim-1 kinase inhibits STAT5-dependent transcription via its interactions with SOCS1 and SOCS3

Katriina J. Peltola, Kirsi Paukku, Teija L. T. Aho, Marja Ruuska, Olli Silvennoinen, and Päivi J. Koskinen

From the Turku Centre for Biotechnology, University of Turku/Åbo Akademi University; the Turku Graduate School of Biomedical Sciences; the Haartman Institute, the Department of Virology; the Biomedicum Helsinki, Programme for Developmental and Reproductive Biology; the Institute of Medical Technology, University of Tampere; and the Department of Clinical Microbiology, Tampere University Hospital, Finland.

Signal transducer and activator of transcription 5 (STAT5) plays a critical role in cytokine-induced survival of hematopoietic cells. One of the STAT5 target genes is pim-1, which encodes an oncogenic serine/threonine kinase. Here we demonstrate that Pim-1 inhibits STAT5-dependent transcription in cells responsive to interleukin-3, prolactin, or erythropoietin. Ectopic expression of Pim-1 in cytokine-dependent FDCP1 myeloid cells results in reduced tyrosine phosphorylation and DNA binding of STAT5, indicating that Pim-1 interferes already with the initial steps of STAT5 activation. However, the Pim-1 kinase does not directly phosphorylate or bind to STAT5. By contrast, Pim-1 interacts with suppressor of cytokine signaling 1 (SOCS1) and SOCS3 and potentiates their inhibitory effects on STAT5, most likely via phosphorylation-mediated stabilization of the SOCS proteins. Thus, both Pim and SOCS family proteins may be components of a negative feedback mechanism that allows STAT5 to attenuate its own activity.


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