Cell cycle, vol. 3(2), 2004, pp. 95-97
Department of Neurobiology and Anatomy
Drexel University College of Medicine
2900 W. Queen Lane, Room186
Hurlin, P., Zhou, Z.-Q., Toyo-oka, K., Ota, S., Walker, W. L., Hirotsune, S., & Wynshaw-Boris, A. (2004). Evidence of Mnt-Myc Antagonism Revealed by Mnt Gene Deletion. Cell Cycle, 3(2), 95–97.
Hurlin, P., Zi-Qiang Zhou, K. Toyo-oka, S. Ota, William L Walker, S. Hirotsune, and A. Wynshaw-Boris. “Evidence of Mnt-Myc Antagonism Revealed by Mnt Gene Deletion.” Cell cycle 3, no. 2 (2004): 95–97.
Hurlin, P., et al. “Evidence of Mnt-Myc Antagonism Revealed by Mnt Gene Deletion.” Cell Cycle, vol. 3, no. 2, 2004, pp. 95–97.
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.