Author(s): Berg T
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Abstract The transcription factor c-Myc is overexpressed in many tumors in human beings and has been identified as a highly promising target for cancer therapy. Most biological functions of c-Myc require heterodimerization with its activation partner Max. Inhibition of the protein-protein interactions between c-Myc and Max by small molecules has been shown to be a feasible and powerful approach toward the inhibition of c-Myc functions. More recently, stabilization of Max homodimers to reduce the amount of Max available for activating c-Myc has also been demonstrated to counteract Myc activity. This review summarizes our current knowledge on small organic molecules that inhibit c-Myc by modulating protein-protein interactions relevant for the biological function of this important oncoprotein.
This article was published in Curr Top Microbiol Immunol
and referenced in Journal of Clinical & Cellular Immunology