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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4308-4316. Prepublished online as a Blood First Edition Paper on February 9, 2006; DOI 10.1182/blood-2005-06-2216. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2216v1 107/11/4308    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Suh, H. C. Articles by Keller, J. R. Search for Related Content PubMed PubMed Citation Articles by Suh, H. C. Articles by Keller, J. R. Related Collections Hematopoiesis and Stem Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS C/EBP determines hematopoietic cell fate in multipotential progenitor cells by inhibiting erythroid differentiation and inducing myeloid differentiation Hyung Chan Suh, John Gooya, Katie Renn, Alan D. Friedman, Peter F. Johnson, and Jonathan R. Keller From the Basic Research Program, Science Applications International Corporation (SAIC)–Frederick, Center for Cancer Research, National Cancer Institute–Frederick, MD; the Division of Pediatric Oncology, Johns Hopkins University, Baltimore, MD; and the Laboratory of Protein Dynamics and Signaling, Center for Cancer Research, National Cancer Institute–Frederick, MD. C/EBP is an essential transcription factor required for myeloid differentiation. While C/EBP can act as a cell fate switch to promote granulocyte differentiation in bipotential granulocyte-macrophage progenitors (GMPs), its role in regulating cell fate decisions in more primitive progenitors is not known. We found increased numbers of erythroid progenitors and erythroid cells in C/EBP–/– fetal liver (FL). Also, enforced expression of C/EBP in hematopoietic stem cells resulted in a loss of erythroid progenitors and an increase in myeloid cells by inhibition of erythroid development and inducing myeloid differentiation. Conditional expression of C/EBP in murine erythroleukemia (MEL) cells induced myeloid-specific genes, while inhibiting erythroid-specific gene expression including erythropoietin receptor (EpoR), which suggests a novel mechanism to determine hematopoietic cell fate. Thus, C/EBP functions in hematopoietic cell fate decisions by the dual actions of inhibiting erythroid and inducing myeloid gene expression in multipotential progenitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. S. Hasemann, I. Damgaard, M. B. Schuster, K. Theilgaard-Monch, A. B. Sorensen, A. Mrsic, T. Krugers, B. Ylstra, F. S. Pedersen, C. Nerlov, et al. Mutation of C/EBP{alpha} predisposes to the development of myeloid leukemia in a retroviral insertional mutagenesis screen Blood, April 15, 2008; 111(8): 4309 - 4321. [Abstract] [Full Text] [PDF] S. Iida, R. Watanabe-Fukunaga, S. Nagata, and R. Fukunaga Essential role of C/EBPalpha in G-CSF-induced transcriptional activation and chromatin modification of myeloid-specific genes. Genes Cells, April 1, 2008; 13(4): 313 - 327. [Abstract] [Full Text] [PDF] D. Wang, J. D'Costa, C. I. Civin, and A. D. Friedman C/EBP{alpha} directs monocytic commitment of primary myeloid progenitors Blood, August 15, 2006; 108(4): 1223 - 1229. [Abstract] [Full Text] [PDF]

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