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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4703-4710. Prepublished online as a Blood First Edition Paper on February 16, 2006; DOI 10.1182/blood-2005-07-2968. This Article Full Text (PDF) All Versions of this Article: 2005-07-2968v1 107/12/4703    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 Vegiopoulos, A. P Articles by Frampton, J. Search for Related Content PubMed PubMed Citation Articles by Vegiopoulos, A. P Articles by Frampton, J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 25, 2005 Accepted February 9, 2006 Coordination of erythropoiesis by the transcription factor c-Myb Alexandros P Vegiopoulos, Paloma Garcia, Nikla Emambokus, and Jon Frampton* Institute of Biomedical Research, The Medical School, University of Birmingham, Birmingham, United Kingdom * Corresponding author; email: j.frampton{at}bham.ac.uk. The involvement of the transcription factor c-Myb in the promotion of proliferation and inhibition of differentiation in erythroid cells has been established in leukemic cell models. The anemic phenotype observed in c-myb knockout and knockdown mice highlights a critical role for c-Myb in erythropoiesis. However, the reason for the failure of erythropoiesis in these mice and the precise function of c-Myb in erythroid progenitors remains elusive. We examined erythroid development under conditions of reduced c-Myb protein levels and demonstrate an unexpected role for c-Myb in the promotion of commitment to the erythroid lineage and progression to erythroblast stages. c-myb knockdown CFU-E stage progenitors displayed an immature phenotype and aberrant expression of several hematopoietic regulators. To extend our findings we analysed the response of normal enriched erythroid progenitors to inducible disruption of a floxed c-myb allele. In agreement with the c-myb knockdown phenotype we show that c-Myb is strictly required for expression of the c-kit receptor in erythroid cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Mithraprabhu and K. L Loveland Control of KIT signalling in male germ cells: what can we learn from other systems? Reproduction, November 1, 2009; 138(5): 743 - 757. [Abstract] [Full Text] [PDF] K. Wahlberg, J. Jiang, H. Rooks, K. Jawaid, F. Matsuda, M. Yamaguchi, M. Lathrop, S. L. Thein, and S. Best The HBS1L-MYB intergenic interval associated with elevated HbF levels shows characteristics of a distal regulatory region in erythroid cells Blood, August 6, 2009; 114(6): 1254 - 1262. [Abstract] [Full Text] [PDF] S. W. Rossi, M.-Y. Kim, A. Leibbrandt, S. M. Parnell, W. E. Jenkinson, S. H. Glanville, F. M. McConnell, H. S. Scott, J. M. Penninger, E. J. Jenkinson, et al. RANK signals from CD4+3 inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla J. Exp. Med., June 11, 2007; 204(6): 1267 - 1272. [Abstract] [Full Text] [PDF] J. Jiang, S. Best, S. Menzel, N. Silver, M. I. Lai, G. L. Surdulescu, T. D. Spector, and S. L. Thein cMYB is involved in the regulation of fetal hemoglobin production in adults Blood, August 1, 2006; 108(3): 1077 - 1083. [Abstract] [Full Text] [PDF]

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