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Blood, 15 July 2008, Vol. 112, No. 2, pp. 308-319. Prepublished online as a Blood First Edition Paper on March 21, 2008; DOI 10.1182/blood-2007-11-115204. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-11-115204v1 112/2/308    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 Zhou, L. Articles by Lowe, J. B. Search for Related Content PubMed PubMed Citation Articles by Zhou, L. Articles by Lowe, J. B. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS AND STEM CELLS Notch-dependent control of myelopoiesis is regulated by fucosylation Lan Zhou1, Lebing Wei Li1, Quanjian Yan1, Bronislawa Petryniak1, Yunfang Man1, Charles Su1, Jeongsup Shim2, Stephanie Chervin3, and John B. Lowe1 1 Department of Pathology, Case Western Reserve University, Cleveland, OH; 2 Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor; and 3 College of Pharmacy, University of Michigan, Ann Arbor Cell-cell contact–dependent mechanisms that modulate proliferation and/or differentiation in the context of hematopoiesis include mechanisms characteristic of the interactions between members of the Notch family of signal transduction molecules and their ligands. Whereas Notch family members and their ligands clearly modulate T lymphopoietic decisions, evidence for their participation in modulating myelopoiesis is much less clear, and roles for posttranslational control of Notch-dependent signal transduction in myelopoiesis are unexplored. We report here that a myeloproliferative phenotype in FX–/– mice, which are conditionally deficient in cellular fucosylation, is consequent to loss of Notch-dependent signal transduction on myeloid progenitor cells. In the context of a wild-type fucosylation phenotype, we find that the Notch ligands suppress myeloid differentiation of progenitor cells and enhance expression of Notch target genes. By contrast, fucosylation-deficient myeloid progenitors are insensitive to the suppressive effects of Notch ligands on myelopoiesis, do not transcribe Notch1 target genes when cocultured with Notch ligands, and have lost the wild-type Notch ligand-binding phenotype. Considered together, these observations indicate that Notch-dependent signaling controls myelopoiesis in vivo and in vitro and identifies a requirement for Notch fucosylation in the expression of Notch ligand binding activity and Notch signaling efficiency in myeloid progenitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Unsweetened Notch leads to myeloproliferation Robert S. Haltiwanger Blood 2008 112: 214-215. [Full Text] [PDF] This article has been cited by other articles: T. Liu, B. Hu, Y. Y. Choi, M. Chung, M. Ullenbruch, H. Yu, J. B. Lowe, and S. H. Phan Notch1 Signaling in FIZZ1 Induction of Myofibroblast Differentiation Am. J. Pathol., May 1, 2009; 174(5): 1745 - 1755. [Abstract] [Full Text] [PDF]

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