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Blood, 1 August 2004, Vol. 104, No. 3, pp. 696-703. Prepublished online as a Blood First Edition Paper on April 1, 2004; DOI 10.1182/blood-2003-05-1754. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-05-1754v1 104/3/696    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 Jacobs-Helber, S. M. Articles by Sawyer, S. T. Search for Related Content PubMed PubMed Citation Articles by Jacobs-Helber, S. M. Articles by Sawyer, S. T. Related Collections Hematopoiesis and Stem Cells Red Cells Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Jun N-terminal kinase promotes proliferation of immature erythroid cells and erythropoietin-dependent cell lines Sarah M. Jacobs-Helber, and Stephen T. Sawyer From the Department of Pharmacology/Toxicology, Virginia Commonwealth University, Richmond, VA. Erythropoietin (EPO) is the hormone necessary for development of erythrocytes from immature erythroid cells. EPO activates Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase (MAPK) family in the EPO-dependent murine erythroid HCD57 cells. Therefore, we tested if JNK activity supported proliferation and/or survival of these cells. Treatment with the JNK inhibitor SP600125 inhibited JNK activity and EPO-dependent proliferation of HCD57 cells and the human EPO-dependent cell lines TF-1 and UT7-EPO. SP600125 also increased the fraction of cells in G2/M. Introduction of a dominant-negative form of JNK1 inhibited EPO-dependent proliferation in HCD57 cells but did not increase the fraction of cells in G2/M. Constitutive JNK activity was observed in primary murine erythroid progenitors. Treatment of primary mouse bone marrow cells with the SP600125 inhibitor reduced the number of erythroid burst-forming units (BFU-e's) but not the more differentiated erythroid colony-forming units (CFU-e's), and SP600125 protected the BFU-e's from apoptosis induced by cytosine arabinoside, demonstrating that the SP600125 inhibited proliferation of the BFU-e's. Therefore, JNK activity appears to be an important regulator of proliferation in immature, primary erythroid cells and 3 erythroid cell lines but may not be required for the survival or proliferation of CFU-e's or proerythroblasts. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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