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Vol. 12, No. 24, pp. 3803-3808, December 15, 1998
Department of Cell Biology, Vanderbilt University School of
Medicine, Nashville, Tennessee 37232-2175 USA;
1 Department of
Molecular Biology, Cell Biology, and Biochemistry, Brown
University, Providence, Rhode Island 02912 USA
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.
[Key Words: c-Myc; transactivation; cell cycle; apoptosis; leaky scanning]
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