Transactivation-defective c-MycS retains the ability to regulate proliferation and apoptosis
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.
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Footnotes
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↵2 Corresponding author.
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E-MAIL steve.hann{at}mcmail.vanderbilt.edu; FAX (615) 343-5791.
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- Received September 24, 1998.
- Accepted November 6, 1998.
- Cold Spring Harbor Laboratory Press