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Repression by the Mad(Mxi1)-Sin3 complex.

N Schreiber-Agus·R A DePinho
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Abstract

The functions of Myc in transformation and transactivation are countered by the suppressive actions of the Mad(Mxi1) family. Mad(Mxi1) proteins not only compete with Myc for dimerization to Max and binding to Myc/Max consensus sites but also recruit powerful repressors of gene expression. A prediction of the yin-yang relationship between Myc and Mad(Mxi1) families would be that the latter constitutes a new class of tumor suppressors. Here, we review the current literature on the Mad(Mxi1) family, with particular attention paid to the molecular mechanisms by which these proteins antagonize the actions of Myc in normal and neoplastic cells.

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AnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBasic Helix-Loop-Helix ProteinsBasic-Leucine Zipper Transcription FactorsBinding SitesBinding, CompetitiveCell Transformation, NeoplasticChromatinConsensus SequenceDNA-Binding ProteinsDimerizationEukaryotic CellsGene Expression RegulationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHistone DeacetylasesMiceMice, KnockoutModels, GeneticMultigene FamilyNeoplasmsNuclear ProteinsNuclear Receptor Co-Repressor 1Proto-Oncogene Proteins c-mycRepressor ProteinsSaccharomyces cerevisiae ProteinsTranscription FactorsTranscriptional ActivationTumor Suppressor ProteinsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.Review

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BibTeXRIS

N Schreiber-Agus, R A DePinho. 1998. Repression by the Mad(Mxi1)-Sin3 complex.. https://doi.org/10.1002/(sici)1521-1878(199810)20%3A10%3C808%3A%3Aaid-bies6%3E3.0.co%3B2-u

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