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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1068-1077. Prepublished online as a Blood First Edition Paper on June 3, 2008; DOI 10.1182/blood-2008-01-133504. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-01-133504v1 112/4/1068    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 Ji, M. Articles by Keller, J. R. Search for Related Content PubMed PubMed Citation Articles by Ji, M. Articles by Keller, J. R. Related Collections Hematopoiesis and Stem Cells Immunobiology Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS AND STEM CELLS Id2 intrinsically regulates lymphoid and erythroid development via interaction with different target proteins Ming Ji1, Huajie Li1, Hyung Chan Suh1, Kimberly D. Klarmann1, Yoshifumi Yokota2, and Jonathan R. Keller1 1 Basic Research Program, SAIC-Frederick, Center for Cancer Research, National Cancer Institute-Frederick, MD; and 2 Department of Biochemistry, Fukui Medical University, Fukui, Japan Inhibitors of DNA binding (Id) family members are key regulators of cellular differentiation and proliferation. These activities are related to the ability of Id proteins to antagonize E proteins and other transcription factors. As negative regulators of E proteins, Id proteins have been implicated in lymphocyte development. Overexpression of Id1, Id2, or Id3 has similar effects on lymphocyte development. However, which Id protein plays a physiologic role during lymphocyte development is not clear. By analyzing Id2 knock-out mice and retroviral transduced hematopoietic progenitors, we demonstrated that Id2 is an intrinsic negative regulator of B-cell development. Hematopoietic progenitor cells overexpressing Id2 did not reconstitute B-cell development in vivo, which resembled the phenotype of E2A null mice. The B-cell population in bone marrow was significantly expanded in Id2 knock-out mice compared with their wild-type littermates. Knock-down of Id2 by shRNA in hematopoietic progenitor cells promoted B-cell differentiation and induced the expression of B-cell lineage–specific genes. These data identified Id2 as a physiologically relevant regulator of E2A during B lymphopoiesis. Furthermore, we identified a novel Id2 function in erythroid development. Overexpression of Id2 enhanced erythroid development, and decreased level of Id2 impaired normal erythroid development. Id2 regulation of erythroid development is mediated via interacting with transcription factor PU.1 and modulating PU.1 and GATA-1 activities. We conclude that Id2 regulates lymphoid and erythroid development via interaction with different target proteins. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Burda, N. Curik, J. Kokavec, P. Basova, D. Mikulenkova, A. I. Skoultchi, J. Zavadil, and T. Stopka PU.1 Activation Relieves GATA-1-Mediated Repression of Cebpa and Cbfb during Leukemia Differentiation Mol. Cancer Res., October 1, 2009; 7(10): 1693 - 1703. [Abstract] [Full Text] [PDF] S. Doulatov, F. Notta, K. L. Rice, L. Howell, A. Zelent, J. D. Licht, and J. E. Dick PLZF is a regulator of homeostatic and cytokine-induced myeloid development Genes & Dev., September 1, 2009; 23(17): 2076 - 2087. [Abstract] [Full Text] [PDF] A. D. Wood, E. Chen, I. J. Donaldson, S. Hattangadi, K. A. Burke, M. A. Dawson, D. Miranda-Saavedra, H. F. Lodish, A. R. Green, and B. Gottgens ID1 promotes expansion and survival of primary erythroid cells and is a target of JAK2V617F-STAT5 signaling Blood, August 27, 2009; 114(9): 1820 - 1830. [Abstract] [Full Text] [PDF]

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