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Blood, 1 April 2004, Vol. 103, No. 7, pp. 2568-2570. Prepublished online as a Blood First Edition Paper on October 23, 2003; DOI 10.1182/blood-2003-06-1803. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-06-1803v1 103/7/2568    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 Kamata, T. Articles by Leavitt, A. D. Search for Related Content PubMed PubMed Citation Articles by Kamata, T. Articles by Leavitt, A. D. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Brief report Raf-1 is not required for megakaryocytopoiesis or TPO-induced ERK phosphorylation Tamihiro Kamata, Catrin A. Pritchard, and Andrew D. Leavitt From the Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA; and the Department of Biochemistry, University of Leicester, Leicester, United Kingdom. Thrombopoietin stimulates extracellular signal-related kinase 1/2 (ERK1/2) phosphorylation in megakaryocytes, and the classic mitogen-activated protein (MAP) kinase (Raf/mitogen-induced extracellular kinase [MEK]/ERK) pathway has been implicated directly and indirectly to play a critical role in megakaryocytopoiesis. However, the involvement of specific Raf family members in megakaryocytopoiesis is unknown. raf-1-/- mice were therefore used to directly determine the role of Raf-1 in megakaryocytopoiesis. Surprisingly, raf-1-/- mice have a modestly higher platelet count than their raf-1+/+ littermates. Nonetheless, the absence of Raf-1 does not alter thrombopoietin-induced expansion of primary megakaryocyte-lineage cells, the development of apoptotic megakaryocytes in the presence or absence of thrombopoietin, or the development of megakaryocyte DNA ploidy distribution. Moreover, raf-1-/- megakaryocytes do not have a compensatory increase in A-Raf or B-Raf expression, and thrombopoietin-induced ERK1/2 phosphorylation is similar in raf-1-/- and raf-1+/+ megakaryocytes. These unexpected findings demonstrate that Raf-1 is dispensable for megakaryocytopoiesis, and for thrombopoietin-induced ERK1/2 activation in primary megakaryocyte-lineage cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. J. S. Stork Unraveling the mysteries of B-Raf: the clot thickens! Blood, August 1, 2005; 106(3): 775 - 776. [Full Text] [PDF] T. Kamata, J. Kang, T.-H. Lee, L. Wojnowski, C. A. Pritchard, and A. D. Leavitt A critical function for B-Raf at multiple stages of myelopoiesis Blood, August 1, 2005; 106(3): 833 - 840. [Abstract] [Full Text] [PDF] S. M. Akula, P. W. Ford, A. G. Whitman, K. E. Hamden, B. A. Bryan, P. P. Cook, and J. A. McCubrey B-Raf-dependent expression of vascular endothelial growth factor-A in Kaposi sarcoma-associated herpesvirus-infected human B cells Blood, June 1, 2005; 105(11): 4516 - 4522. [Abstract] [Full Text] [PDF]

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