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This Article Full Text Full Text (PDF) 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 Karafiát, V. Articles by Dvorák, M. Search for Related Content PubMed PubMed Citation Articles by Karafiát, V. Articles by Dvorák, M. Related Collections Hematopoiesis and Stem Cells Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 December 2001, Vol. 98, No. 13, pp. 3668-3676 HEMATOPOIESIS The leucine zipper region of Myb oncoprotein regulates the commitment of hematopoietic progenitors Vít Karafiát, Marta Dvoáková, Petr Pajer, Jarmila Králová, Zuzana Hoejí, Vladimír ermák, Petr Bartnk, Martin Zenke, and Michal Dvoák From the Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, and the Max-Delbrück Center for Molecular Medicine, Berlin, Germany. The development of blood cells proceeds from pluripotent stem cells through multipotent progenitors into mature elements belonging to at least 8 different lineages. The lineage choice process during which stem cells and progenitors commit to a particular lineage is regulated by a coordinated action of extracellular signals and transcription factors. Molecular mechanisms controlling commitment are largely unknown. Here, the transcription factor v-Myb and its leucine zipper region (LZR) are identified as regulators of the commitment of a common myeloid progenitor and progenitors restricted to the myeloid lineage. It is demonstrated that wild-type v-Myb with the intact LZR directs development of progenitors into the macrophage lineage. Mutations in this region compromise commitment toward myeloid cells and cause v-Myb to also support the development of erythroid cells, thrombocytes, and granulocytes, similar to the c-Myb protein. In agreement with that, the wild-type v-Myb induces high expression of myeloid factors C/EBP, PU.1, and Egr-1 in its target cells, whereas SCL, GATA-1, and c-Myb are more abundant in cells expressing the v-Myb LZR mutant. It is proposed that Myb LZR can function as a molecular switch, affecting expression of lineage-specifying transcription factors and directing the development of hematopoietic progenitors into either myeloid or erythroid lineages. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K.-R. Koh, M. Janz, M. Y. Mapara, B. Lemke, D. Stirling, B. Dorken, M. Zenke, and S. Lentzsch Immunomodulatory derivative of thalidomide (IMiD CC-4047) induces a shift in lineage commitment by suppressing erythropoiesis and promoting myelopoiesis Blood, May 15, 2005; 105(10): 3833 - 3840. [Abstract] [Full Text] [PDF] K. M. McNagny and T. Graf E26 leukemia virus converts primitive erythroid cells into cycling multilineage progenitors Blood, February 1, 2003; 101(3): 1103 - 1110. [Abstract] [Full Text] [PDF] H. Gao, S. Parkin, P. F. Johnson, and R. C. Schwartz C/EBPgamma Has a Stimulatory Role on the IL-6 and IL-8 Promoters J. Biol. Chem., October 4, 2002; 277(41): 38827 - 38837. [Abstract] [Full Text] [PDF]

	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020