SEARCH:   Advanced

Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2001-12-0236. This Article Full Text 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 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 Aittomäki, S. Articles by Silvennoinen, O. Search for Related Content PubMed PubMed Citation Articles by Aittomäki, S. Articles by Silvennoinen, O. Related Collections Signal Transduction Gene Expression Brief Reports Hematopoiesis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 August 2002, Vol. 100, No. 3, pp. 1078-1080 BRIEF REPORT Distinct functions for signal transducer and activator of transcription 1 and PU.1 in transcriptional activation of Fc  receptor I promoter Saara Aittomäki, Jie Yang, Edward W. Scott, M. Celeste Simon, and Olli Silvennoinen From the Institute of Medical Technology, University of Tampere, Finland; the Department of Molecular Genetics and Microbiology, Shands Cancer Center, University of Florida, Gainesville; the Abramson Family Cancer Research Institute, Howard Hughes Medical Institute, University of Pennsylvania Cancer Center, Philadelphia; and the Department of Clinical Microbiology, Tampere University Hospital, Finland. The myeloid cell-specific expression and interferon- (IFN-) induction of Fc  receptor I (FcRI) requires cooperation between PU.1 and signal transducer and activator of transcription 1 (Stat1) by means of mechanisms that are unknown. We found that PU.1 and Stat1 mediated distinct functions in the activation of FcRI promoter. 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 CREB-binding protein (CBP)/p300. These results define functional cooperativity between PU.1 and Stat1 in FcRI promoter activation, in which PU.1 appears to serve as a bridging factor with the basal transcription machinery and IFN--mediated induction of transcription occurs through recruitment of CBP/p300 by Stat1. © 2002 by The American Society of Hematology.   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]

	Blood Online is supported in part by Genentech BioOncology and Biogen Idec
	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020