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Blood, 15 November 2007, Vol. 110, No. 10, pp. 3618-3623. Prepublished online as a Blood First Edition Paper on August 15, 2007; DOI 10.1182/blood-2007-06-097030. This Article Full Text (PDF) All Versions of this Article: blood-2007-06-097030v1 110/10/3618    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 Wu, L. Articles by Griffin, J. D. Search for Related Content PubMed PubMed Citation Articles by Wu, L. Articles by Griffin, J. D. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 21, 2007 Accepted August 11, 2007 The transcriptional co-activator Maml1 is required for Notch2-mediated marginal zone B cell development Lizi Wu*, Ivan Maillard, Makoto Nakamura, Warren S. Pear, and James D. Griffin Department of Molecular Genetics and Microbiology, Shands Cancer Center, University of Florida, Gainesville, FL, United States Division of Hematology-Oncology, University of Pennsylvania School of Medicine, Philadelphia, PA, United States Department of Medical Oncology, Dana-Farber Cancer Institute, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States Department of Pathology & Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, United States * Corresponding author; email: lzwu{at}ufl.edu. Signaling mediated by various Notch receptors and their ligands regulates diverse biological processes, including lymphoid cell fate decisions. Notch1 is required during T cell development, while Notch2 and the Notch ligand Delta-like1 control marginal zone B (MZB) cell development. We previously determined that Mastermind-like (MAML) transcriptional co-activators are required for Notch-induced transcription by forming ternary nuclear complexes with Notch and the transcription factor CSL. The three MAML family members (MAML1-3) are collectively essential for Notch activity in vivo, but whether individual MAMLs contribute to the specificity of Notch functions is unknown. Here, we addressed this question by studying lymphopoiesis in the absence of the Maml1 gene. Since Maml1-/- mice suffered perinatal lethality, hematopoietic chimeras were generated with Maml1-/-, Maml1+/- or wild-type fetal liver progenitors. Maml1 deficiency minimally affected T cell development, but was required for the development of MZB cells, similar to the phenotype of Notch2 deficiency. Moreover, the number of MZB cells correlated with Maml1 gene dosage. Since all three Maml genes were expressed in MZB cells and their precursors, these results suggest that Maml1 is specifically required for Notch2 signaling in MZB cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D.-M. Shin, D. J. Shaffer, H. Wang, D. C. Roopenian, and H. C. Morse III NOTCH Is Part of the Transcriptional Network Regulating Cell Growth and Survival in Mouse Plasmacytomas Cancer Res., November 15, 2008; 68(22): 9202 - 9211. [Abstract] [Full Text] [PDF]

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