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Blood, 1 July 2007, Vol. 110, No. 1, pp. 107-115. Prepublished online as a Blood First Edition Paper on March 14, 2007; DOI 10.1182/blood-2006-08-039628. This Article Full Text (PDF) All Versions of this Article: blood-2006-08-039628v1 110/1/107    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 Tanaka, Y. Articles by Kawamata, S. Search for Related Content PubMed PubMed Citation Articles by Tanaka, Y. Articles by Kawamata, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 21, 2006 Accepted March 11, 2007 Forced expression of Nanog in hematopoietic stem cells results in a T cell disorder Yosuke Tanaka, Takumi Era, Shin-ichi Nishikawa, and Shin Kawamata* Riken Center for Developmental Biology, Kobe, Japan Foundation for Biomedical Research & Innovation, Kobe, Japan * Corresponding author; email: kawamata{at}fbri.org. Nanog is a key molecule involved in the maintenance of the self-renewal of undifferentiated ES cells. In this work we investigate whether Nanog has the ability to enhance self-renewal in hematopoietic stem cells. Contrary to our expectation, no positive effect of Nanog transduction was detected in bone marrow reconstitution assays. However, recipients of nanog-transduced (Nanog°) HSC invariantly develop a unique disorder typified by an atrophic thymus occupied by Nanog-expressing TCR+ cells (Nanog°T cells). All thymi are eventually occupied by Nanog°T cells with CD25+CD44+ surface phenotype, home selectively to the thymus upon transfer, and suppress normal thymocyte development, which is partly ascribed to destruction of the microenvironment in the thymus cortex. Moreover, this initial disorder invariantly develops to a lymphoproliferative disorder, in which Nanog°T cells undergo unlimited proliferation in the peripheral lymphoid tissues and eventually kill the host. This invariable end-result suggests that Nanog is a candidate oncogene for T cell malignancy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. S. You, J. K. Kang, D.-W. Seo, J. H. Park, J. W. Park, J. C. Lee, Y. J. Jeon, E. J. Cho, and J.-W. Han Depletion of Embryonic Stem Cell Signature by Histone Deacetylase Inhibitor in NCCIT Cells: Involvement of Nanog Suppression Cancer Res., July 15, 2009; 69(14): 5716 - 5725. [Abstract] [Full Text] [PDF] X. Zhang, I. Neganova, S. Przyborski, C. Yang, M. Cooke, S. P. Atkinson, G. Anyfantis, S. Fenyk, W. N. Keith, S. F. Hoare, et al. A role for NANOG in G1 to S transition in human embryonic stem cells through direct binding of CDK6 and CDC25A J. Cell Biol., January 12, 2009; 184(1): 67 - 82. [Abstract] [Full Text] [PDF]

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