Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3

A study of the factors that facilitate Mad-Max transcriptional inhibition reveals that the repression occurs through the anchoring of mSin3 to DNA as corepressors and indicates the preservation of the transcriptional repression from yeast to mammals. Two mammalian cDNAs that code for Mad-binding proteins exhibit sequence homology with Sin3 and possess four conserved paired amphipathic helix domains. The Mad-Max E box-binding site is identified by ternary complexes formed by Mad-Max and mSin3. Interactions with mSin3 proteins are abolished and Mad transcriptional repression is inhibited by point mutations in the amphipathic alpha-helical region.