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

Xiao Q, Claassen G, Shi J, Adachi S, Sedivy J, Hann SR
Genes Dev. 1998 12 (24): 3803-8

PMID: 9869633 · PMCID: PMC317265 · DOI:10.1101/gad.12.24.3803

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.

MeSH Terms (27)

3T3 Cells Animals Apoptosis Cell Division Cell Line Cell Transformation, Neoplastic Enhancer Elements, Genetic Gene Expression Regulation Genes, myc Genes, p53 Intracellular Signaling Peptides and Proteins Membrane Glycoproteins Mice Ornithine Decarboxylase Phenotype Protein Isoforms Protein Precursors Proteins Proto-Oncogene Proteins c-myc Rats Repressor Proteins Response Elements Saccharomyces cerevisiae Proteins Sequence Deletion Thymosin Transcriptional Activation Transfection

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