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Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2001-12-0236. This Article Full Text (PDF) All Versions of this Article: 2001-12-0236v1 100/3/1078    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 Aittomaki, S. Articles by Silvennoinen, O. Search for Related Content PubMed PubMed Citation Articles by Aittomaki, S. Articles by Silvennoinen, O. Social Bookmarking                   What's this? Submitted December 13, 2001 Accepted March 26, 2002 Distinct functions for Stat1 and PU.1 in transcriptional activation of FcRI promoter Saara Aittomaki, Jie Yang, Edward W Scott, M. Celeste Simon, and Olli Silvennoinen* Institute of Medical Technology, University of Tampere, Tampere, Finland; Clinical Microbiology, Tampere University Hospital, Tampere, Finland Institute of Medical Technology, University of Tampere, Tampere, Finland Department of Molecular Genetics and Microbiology, Shands Cancer Center, University of Florida, Gainesville, Florida, USA Abramson Family Cancer Research Institute, Howard Hughes Medical Institute, University of Pennsylvania Cancer Center, Philadelphia, PA, USA Institute of Medical Technology, University of Tampere, Tampere, Finland; Department of Clinical Microbiology, Tampere University Hospital, Tampere, Finland * Corresponding author; email: olli.silvennoinen{at}uta.fi. The myeloid cell-specific expression and interferon- (IFN-) induction of FcRI requires cooperation between PU.1 and Stat1 by unknown mechanisms. PU.1 and Stat1 were found to mediate distinct functions in FcRI promoter activation. The basal activity of the natural FcRI promoter was strictly dependent on PU.1, and IFN- induction required both PU.1 and Stat1. Recruitment of TATA binding protein (TBP) to the FcRI promoter did not replace PU.1 in promoter activation suggesting that TBP is not sufficient for FcRI activation and that PU.1 mediates additional contacts with basal transcription machinery. In contrast, Stat1 did not interact with basal transcription machinery, but the Stat1-mediated activation of FcRI promoter critically required CBP/p300. These results define functional cooperativity between PU.1 and Stat1 in FcRI promoter activation where PU.1 appears to serve as a bridging factor with the basal transcription machinery, and the IFN- mediated induction of transcription occurs through recruitment of CBP/p300 by Stat1. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Dahl, S. R. Iyer, K. S. Owens, D. D. Cuylear, and M. C. Simon The Transcriptional Repressor GFI-1 Antagonizes PU.1 Activity through Protein-Protein Interaction J. Biol. Chem., March 2, 2007; 282(9): 6473 - 6483. [Abstract] [Full Text] [PDF] D. M. Barrett, K. S. Gustafson, J. Wang, S. Z. Wang, and G. D. Ginder A GATA Factor Mediates Cell Type-Restricted Induction of HLA-E Gene Transcription by Gamma Interferon Mol. Cell. Biol., July 15, 2004; 24(14): 6194 - 6204. [Abstract] [Full Text] [PDF] S. Aittomaki, J. Yang, E. W. Scott, M. C. Simon, and O. Silvennoinen Molecular basis of Stat1 and PU.1 cooperation in cytokine-induced Fc{gamma} receptor I promoter activation Int. Immunol., February 1, 2004; 16(2): 265 - 274. [Abstract] [Full Text] [PDF]

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