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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3396-3404. Prepublished online as a Blood First Edition Paper on August 4, 2005; DOI 10.1182/blood-2005-04-1739. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-04-1739v1 106/10/3396    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 Bonnesen, B. Articles by Labuda, T. Search for Related Content PubMed PubMed Citation Articles by Bonnesen, B. Articles by Labuda, T. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 28, 2005 Accepted July 3, 2005 MEK kinase 1 activity is required for definitive erythropoiesis in the mouse fetal liver Barbara Bonnesen, Cathrine Orskov, Susanne Rasmussen, Peter J Holst, Jan P Christensen, Karsten W Eriksen, Klaus Qvortrup, Niels Odum, and Tord Labuda* Institute of Molecular Biology and Physiology, Department of Immunology, University of Copenhagen, Copenhagen, Denmark Department of Medical Anatomy, University of Copenhagen, Cpenhagen, Denmark Department of Medical Microbiology and immunology, University of Copenhagen, Copenhagen, Denmark Department of Medical Pharmacology, University of Copenhagen, Copenhagen, Denmark Institute of Molecular Biology and Physiology, Department of Immunology, University of Copenhagen, Copenhagen, Denmark; Department of Medical Microbiology and immunology, University of Copenhagen, Copenhagen, Denmark * Corresponding author; email: t.labuda{at}immi.ku.dk. MEKK1 is a JNK activating kinase known to be implicated in proinflammatory responses and cell motility. Using mice deficient for MEKK1 kinase activity (Mekk1KD) we show a role for MEKK1 in definitive mouse erythropoiesis. Although Mekk1KD mice are alive and fertile on a 129 x C57/BL6 background the frequency of Mekk1KD embryos that develop past E14.5 is dramatically reduced when backcrossed into the C57/BL6 background. At E13.5 Mekk1KD embryos have normal morphology but are anemic due to failure of definitive erythropoiesis. When Mekk1KD fetal liver cells were transferred to lethally irradiated wild-type hosts, mature red blood cells were generated from the mutant cells, suggesting that MEKK1 functions in a non-cell autonomous manner. Based on Immunohistochemical and hemoglobin-chain-transcription analysis we propose that the failure of definitive erythropoiesis is due to a deficiency in enucleation activity caused by insufficient macrophage mediated nuclear DNA destruction. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. R. Geest and P. J. Coffer MAPK signaling pathways in the regulation of hematopoiesis J. Leukoc. Biol., August 1, 2009; 86(2): 237 - 250. [Abstract] [Full Text] [PDF] S. Soni, S. Bala, B. Gwynn, K. E. Sahr, L. L. Peters, and M. Hanspal Absence of Erythroblast Macrophage Protein (Emp) Leads to Failure of Erythroblast Nuclear Extrusion J. Biol. Chem., July 21, 2006; 281(29): 20181 - 20189. [Abstract] [Full Text] [PDF]

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