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Blood, 1 November 2007, Vol. 110, No. 9, pp. 3150-3157. Prepublished online as a Blood First Edition Paper on August 6, 2007; DOI 10.1182/blood-2007-05-092262. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-05-092262v1 110/9/3150    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 Mora-López, F. Articles by Campos-Caro, A. Search for Related Content PubMed PubMed Citation Articles by Mora-López, F. Articles by Campos-Caro, A. Related Collections Hematopoiesis and Stem Cells Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Human BSAP and BLIMP1 conform an autoregulatory feedback loop Francisco Mora-López1, Elena Reales1, José A. Brieva1, and Antonio Campos-Caro1 1 Unidad de Investigación, Hospital Universitario Puerta del Mar, Cádiz, Spain B-lymphocyte–induced maturation protein-1 (BLIMP1), encoded by the PRDM1 gene, is a transcriptional repressor considered a master regulator that is required and sufficient for plasma cell (PC) differentiation. BLIMP1 represses the PAX5 gene, coding for the B-cell lineage–specific activator protein (BSAP), which is required for B-cell identity and survival. Mutations in PAX5 gene as well as in PRDM1 gene have been recently implicated in lymphomas. In the present study, sequence analysis of PRDM1 gene revealed a binding site for BSAP transcription factor. By analyzing different human cell lines, we have found that a specific nuclear factor for B-cell lines binds to a site on the PRDM1 promoter. Electrophoretic mobility shift assays identified this factor as BSAP, and chromatin immunoprecipitation assays confirmed its binding in vivo to the human PRDM1 promoter. Moreover, by ectopically expressing BSAP, and using a PRDM1 promoter with the BSAP-binding site mutated, we demonstrated that this factor represses the expression of BLIMP1. Therefore, repression of PRDM1 by BSAP reveals an autoregulatory negative-feedback loop that could play a relevant role in controlling human PC differentiation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. A. J. Morgan, E. Magnusdottir, T. C. Kuo, C. Tunyaplin, J. Harper, S. J. Arnold, K. Calame, E. J. Robertson, and E. K. Bikoff Blimp-1/Prdm1 Alternative Promoter Usage during Mouse Development and Plasma Cell Differentiation Mol. Cell. Biol., November 1, 2009; 29(21): 5813 - 5827. [Abstract] [Full Text] [PDF] D. Schneider, M. A. Manzan, B. S. Yoo, R. B. Crawford, and N. Kaminski Involvement of Blimp-1 and AP-1 Dysregulation in the 2,3,7,8-Tetrachlorodibenzo-p-dioxin-mediated Suppression of the IgM Response by B Cells Toxicol. Sci., April 1, 2009; 108(2): 377 - 388. [Abstract] [Full Text] [PDF] V. L. Bryant, C. S. Ma, D. T. Avery, Y. Li, K. L. Good, L. M. Corcoran, R. de Waal Malefyt, and S. G. Tangye Cytokine-Mediated Regulation of Human B Cell Differentiation into Ig-Secreting Cells: Predominant Role of IL-21 Produced by CXCR5+ T Follicular Helper Cells J. Immunol., December 15, 2007; 179(12): 8180 - 8190. [Abstract] [Full Text] [PDF]

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