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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4200-4208. Prepublished online as a Blood First Edition Paper on January 25, 2007; DOI 10.1182/blood-2006-08-044149. This Article Full Text (PDF) All Versions of this Article: blood-2006-08-044149v1 109/10/4200    most recent Alert me when this article is cited Alert me if a correction is posted 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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Koga, S. Articles by Minegishi, N. Search for Related Content PubMed PubMed Citation Articles by Koga, S. Articles by Minegishi, N. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 28, 2006 Accepted January 15, 2007 Cell cycle-dependent oscillation of GATA2 expression in hematopoietic cells Shinichiro Koga, Nobuhiro Yamaguchi, Tomoko Abe, Masayoshi Minegishi, Shigeru Tsuchiya, Masayuki Yamamoto, and Naoko Minegishi* Tohuku University Biomedical Engineering Research Org., Dept of Pediatrics, Graduate School of Medicine, Tohoku University, Sendai, Japan Division of Blood Transfusion, Tohoku University Hospital, Sendai, Japan Graduate School of Comprehensive Human Science, University of Tsukuba, Tsukuba, Japan * Corresponding author; email: nmine{at}tubero.tohoku.ac.jp. In vitro manipulation of hematopoietic stem cells (HSC) is a key issue in both transplantation therapy and regenerative medicine, and thus new methods are required to achieve HSC expansion with self-renewal. GATA2 is a transcription factor controlling the pool size of HSC. Interestingly, continuous overexpression of GATA2 does not induce HSC proliferation. In this report, we demonstrate that GATA2 expression, in leukemic and normal hematopoietic cells, oscillates during the cell cycle, such that expression is high in S phase but low in G1/S and M phase. GATA2 binding to target Bcl-X gene also oscillates in accordance with GATA2 expression. Using a green fluorescent protein (GFP)-GATA2 fusion protein, we demonstrate cell cycle-specific activity of proteasome-dependent degradation of GATA2. Immunoprecipitation/immunoblotting analysis demonstrated phosphorylation of GATA2 at cyclin dependent kinase (Cdk)-consensus motifs, S/T 0P+1 and interaction of GATA2 with Cdk2/cyclin A2. Cdk2/cyclin A2, and Cdk4/cyclin D1 phosphorylated GATA2 in vitro. Mutants in phosphorylation motifs exhibited altered expression profiles of GFP-GATA2 domain fusion proteins. These results indicate that GATA2 phosphorylation by Cdk/cyclin systems is responsible to the cell cycle-dependent regulation of GATA2 expression, and suggest the possibility that a cell cycle-specific "on-off" response of GATA2 expression may control hematopoietic cell proliferation and survival. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Minegishi, H. Harigae, and M. Yamamoto Bidirectional Control of Transcription Factor GATA2 and Cyclin/Cdks in Hematopoietic Cells. Blood (ASH Annual Meeting Abstracts), November 16, 2008; 112(11): 1382 - 1382. [Abstract] R. S. Viger, S. M. Guittot, M. Anttonen, D. B. Wilson, and M. Heikinheimo Role of the GATA Family of Transcription Factors in Endocrine Development, Function, and Disease Mol. Endocrinol., April 1, 2008; 22(4): 781 - 798. [Abstract] [Full Text] [PDF]

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