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First published online January 12, 2006
doi: 10.1242/10.1242/jcs.02815

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Of Myc and Mnt

Shriners Hospitals for Children and Department of Cell and Developmental Biology, Oregon Health and Science University, 3101 SW Sam Jackson Park Rd, Portland, OR 97239, USA

^* Author for correspondence (e-mail: pjh{at}shcc.org)

Accepted 29 November 2005

Deregulation of Myc expression is a common feature in cancer and leads to tumor formation in experimental model systems. There are several potential barriers that Myc must overcome in order to promote tumorigenesis, including its propensity to sensitize many cell types to apoptotic cell death. Myc activities appear also to be constrained and fine-tuned by a set of proteins that include the Mxd (formerly named Mad) family and the related protein Mnt. Like Myc-family proteins, Mxd and Mnt proteins use Max as a cofactor for DNA binding. But Mnt-Max and Mxd-Max complexes are transcriptional repressors and can antagonize the transcriptional activation function of Myc-Max. Studies examining the relationship between Myc, Mxd and Mnt proteins suggest that whereas Mnt plays a general role as a Myc antagonist, Mxd proteins have more specialized roles as Myc antagonist that is probably related to their more restricted expression patterns. The interplay between these proteins is postulated to fine-tune Myc activity for cell-cycle entry and exit, proliferation rate and apoptosis.

Key words: Myc, Mnt, Mad, Mxd, Max, Cell cycle, Cancer

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