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Negative regulation of STAT92E by an N-terminally truncated STAT protein derived from an alternative promoter site

Genes & Dev., 15 September 2002
Vol. 16, Issue 18, p. 2379-2389
DOI: 10.1101/gad.1020702

Negative regulation of STAT92E by an N-terminally truncated STAT protein derived from an alternative promoter site

  1. Melissa A. Henriksen1,
  2. Aurel Betz1,
  3. Marc V. Fuccillo, and
  4. James E. Darnell, Jr.2
  1. Laboratory of Molecular Cell Biology, The Rockefeller University, New York, New York 10021, USA


Previously unrecognized mRNAs originating from a dual promoter at the stat92E locus are described. One of these encodes a truncated protein, ΔNSTAT92E, that lacks the N-terminal 133 amino acids. Antibodies detect both the full-length and truncated molecules early in embryogenesis (1–5 h), and mRNA detection by specific RT-PCR reactions accords with the protein distribution. Given that the N termini of mammalian STATs are known to have positive functions in transcriptional activation, we explored the role of ΔNSTAT92E early in embryogenesis. By increasing the ΔNSTAT92E-to-STAT92E ratio in overexpression and RNAi experiments, we observe phenotypes compatible with suppression of wild-type STAT92E activity. We therefore conclude that the short form of STAT92E is a naturally occurring dominant-negative product that can be added to the growing list of negative regulators of STAT activity.

  • Drosophila melanogaster
  • STAT92E
  • alternative promoters
  • differential splicing


  • 1 These authors contributed equally to this work.

  • 2 Corresponding author.

  • E-MAIL darnell{at}; FAX (212) 327-8801.

  • Article and publication are at

    • Received July 2, 2002.
    • Accepted July 18, 2002.


M. A. Henriksen, A. Betz, M. V. Fuccillo, and J. E. Darnell, Negative regulation of STAT92E by an N-terminally truncated STAT protein derived from an alternative promoter site. Genes & Dev. 16, 2379-2389 (2002).

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