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Blood, 12 February 2009, Vol. 113, No. 7, pp. 1455-1463. Prepublished online as a Blood First Edition Paper on September 25, 2008; DOI 10.1182/blood-2008-05-159905. This Article Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2008-05-159905v1 113/7/1455    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 Zhang, Y. Articles by Killeen, N. Search for Related Content PubMed PubMed Citation Articles by Zhang, Y. Articles by Killeen, N. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 27, 2008 Accepted September 7, 2008 Mll5 contributes to hematopoietic stem cell fitness and homeostasis Yan Zhang, Jasmine Wong, Mark Klinger, Mary T. Tran, Kevin M Shannon, and Nigel Killeen* Department of Microbiology and Immunology, University of California San Francisco, San Francisco, CA, United States Department of Pediatrics, University of California San Francisco, San Francisco, CA, United States * Corresponding author; email: nigel.killeen{at}ucsf.edu. MLL5 is a novel trithorax group gene and a candidate tumor suppressor gene located within a 2.5 Mb interval of chromosome band 7q22 that is frequently deleted in human myeloid malignancy. Here we show that inactivation of the Mll5 gene in mice results in a 30% reduction in the average representation of hematopoietic stem cells, and in functional impairment of long-term hematopoietic repopulation potential under competitive conditions. Bone marrow cells from Mll5-deficient mice were defective in spleen colony-forming assays, and the mutant mice showed enhanced susceptibility to 5-Fluorouracil-induced myelosuppression. Heterozygous and homozygous Mll5 mutant mice did not spontaneously develop hematologic cancers, and loss of Mll5 did not alter the phenotype of a fatal myeloprolferative disorder induced by oncogenic Kras in vivo. Collectively, the data reveal an important role for Mll5 in HSC homeostasis, and provide a basis for further studies to explore its role in leukemogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: MLL5 governs hematopoiesis: a step closer Han Liu, Todd D. Westergard, and James J.-D. Hsieh Blood 2009 113: 1395-1396. [Full Text] [PDF] This article has been cited by other articles: S. Sebastian, P. Sreenivas, R. Sambasivan, S. Cheedipudi, P. Kandalla, G. K. Pavlath, and J. Dhawan MLL5, a trithorax homolog, indirectly regulates H3K4 methylation, represses cyclin A2 expression, and promotes myogenic differentiation PNAS, March 24, 2009; 106(12): 4719 - 4724. [Abstract] [Full Text] [PDF] H. Liu, T. D. Westergard, and J. J.-D. Hsieh MLL5 governs hematopoiesis: a step closer Blood, February 12, 2009; 113(7): 1395 - 1396. [Full Text] [PDF]

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