MYC and its family of related transcription factors are central to cell growth, proliferation, metabolism and apoptosis. Deregulated expression of MYC drives most human cancers.  

MNT antagonizes MYC by binding to MYC’s obligate DNA binding partner MAX. We have found that MYC-driven lymphomagenesis is slowed in a MNT+/- background, a phenotype consistent with increased susceptibility to apoptosis. We are now using conditional deletion to further reduce MNT levels and determine the impact on cell proliferation and apoptosis.