Transactivation-defective c-MycS retains the ability to regulate proliferation and apoptosis

  1. Qiurong Xiao,
  2. Gisela Claassen,
  3. Jingyu Shi,
  4. Susumu Adachi1,
  5. John Sedivy1, and
  6. Stephen R. Hann2
  1. Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2175 USA; 1Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912 USA

Abstract

Transcriptional activation by c-Myc through specific E box elements is thought to be essential for its biological role. However, c-MycS is unable to activate transcription through these elements and yet retains the ability to stimulate proliferation, induce anchorage-independent growth, and induce apoptosis. In addition, c-MycS retains the ability to repress transcription of several specific promoters. Furthermore, c-MycS can rescue the c-myc null phenotype in fibroblasts with homozygous deletion of c-myc. Taken together, our data argue against the paradigm that all of the biological functions of c-Myc are mediated by transcriptional activation of specific target genes through E box elements.

Keywords

Footnotes

  • 2 Corresponding author.

  • E-MAIL steve.hann{at}mcmail.vanderbilt.edu; FAX (615) 343-5791.

    • Received September 24, 1998.
    • Accepted November 6, 1998.
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