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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 Snow, J. W. Articles by Goldsmith, M. A. Search for Related Content PubMed PubMed Citation Articles by Snow, J. W. Articles by Goldsmith, M. A. Related Collections Hematopoiesis and Stem Cells Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 January 2002, Vol. 99, No. 1, pp. 95-101 HEMATOPOIESIS STAT5 promotes multilineage hematolymphoid development in vivo through effects on early hematopoietic progenitor cells Jonathan W. Snow, Ninan Abraham, Melissa C. Ma, Nancy W. Abbey, Brian Herndier, and Mark A. Goldsmith From the Gladstone Institute of Virology and Immunology, Departments of Microbiology and Immunology, Pathology, and Medicine, University of California at San Francisco, San Francisco, CA. The transcription factor signal transducers and activators of transcription 5 (STAT5) is activated by numerous cytokines that orchestrate blood cell development. Multilineage peripheral blood cytopenias were observed in adult mice lacking both isoforms of STAT5 (STAT5A and STAT5B) as well as accelerated rates of apoptosis in the bone marrow. Although the hematopoietic stem cell (HSC) population was preserved in a number of these mice, the post-HSC progenitor populations were diminished and a marked reduction in functional progenitors (spleen colony-forming units) was detected. Competitive bone marrow transplantation studies in vivo revealed a profound impairment of repopulation potential of STAT5-null HSCs, leading to complete lack of contribution to the myeloid, erythroid, and lymphoid lineages. These abnormalities were associated with heightened proliferation activity in the HSC fraction, suggesting the action of homeostatic mechanisms to maintain sufficient levels of diverse blood cell types for viability. Thus, STAT5 normally sustains the robust hematopoietic reserve that contributes to host viability through crucial survival effects on early progenitor cells. © 2002 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. Ohmori, Y. Luo, Y. Jia, J. Nishida, Z. Wang, K. D. Bunting, D. Wang, and H. 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	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020