Brief report Distinct functions for signal transducer and activator of transcription 1 and PU.1 in transcriptional activation of Fc receptor I promoter

نویسندگان

  • Saara Aittomäki
  • Jie Yang
  • Edward W. Scott
  • Olli Silvennoinen
چکیده

The myeloid cell–specific expression and interferon(IFN) induction of Fc receptor I (Fc RI) 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 Fc RI promoter. The basal activity of the natural Fc RI promoter was strictly dependent on PU.1, and IFNinduction required both PU.1 and Stat1. Recruitment of TATA-binding protein (TBP) to the Fc RI promoter did not replace PU.1 in promoter activation, suggesting that TBP is not sufficient for Fc RI 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 Fc RI promoter critically required CREBbinding protein (CBP)/p300. These results define functional cooperativity between PU.1 and Stat1 in Fc RI promoter activation, in which PU.1 appears to serve as a bridging factor with the basal transcription machinery and IFN–mediated induction of transcriptionoccurs throughrecruitmentofCBP/ p300 by Stat1. (Blood. 2002;100:1078-1080)

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تاریخ انتشار 2002