Evidence of Mnt-Myc antagonism revealed by Mnt gene deletion

Abstract

Myc proteins play a central role in promoting cell proliferation and contribute to a diverse array of cancers. Myc function appears completely dependent on heterodimerization with Max through related bHLHZip regions. Max interaction with Myc is required for DNA binding at so-called E-box sequences and Myc-dependent transcriptional activation. The identification of Mnt as a ubiquitously expressed Max-interacting transcriptional repressor with similar DNA binding specificity raised the possibility that Mnt may serve a general role as a Myc antagonist.