Role for N-CoR and histone deacetylase in Sin3-mediated transcriptional repression

Normal mammalian growth and development are highly dependent on the regulation of the expression and activity of the Myc family of transcription factors. Mxi1-mediated inhibition of Myc activities requires interaction with mammalian Sln3A or Sin3B proteins, which have been purported to act as scaffo...

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Bibliographic Details
Published in:Nature (London) 1997-05, Vol.387 (6628), p.49-55
Main Authors: Alland, Lelia, Muhle, Rebecca, Hou, Harry, Potes, Jason, Chin, Lynda, Schreiber-Agus, Nicole, DePinho, Ronald A
Format: Article
Language:English
Subjects:
3T3 Cells
Animals
Basic Helix-Loop-Helix Transcription Factors
Biological and medical sciences
DNA-Binding Proteins - physiology
Fundamental and applied biological sciences. Psychology
Fungal Proteins - physiology
Gene Expression Regulation
Genes, myc
Genetics
Histone Deacetylases - physiology
Humanities and Social Sciences
Humans
Mammals
Mice
Microbiology
Molecular and cellular biology
Molecular genetics
multidisciplinary
Nuclear Proteins - physiology
Nuclear Receptor Co-Repressor 1
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
Repressor Proteins - physiology
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae Proteins
Science
Science (multidisciplinary)
Transcription Factors - physiology
Transcription, Genetic
Transcription. Transcription factor. Splicing. Rna processing
Tumor Suppressor Proteins
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Summary:Normal mammalian growth and development are highly dependent on the regulation of the expression and activity of the Myc family of transcription factors. Mxi1-mediated inhibition of Myc activities requires interaction with mammalian Sln3A or Sin3B proteins, which have been purported to act as scaffolds for additional co-repressor factors. The identification of two such Sin3-associated factors, the nuclear receptor co-repressor (N-CoR) and histone deacetylase (HD1), provides a basis for Mxi1/Sin3-induced transcriptional repression and tumour suppression.
ISSN:0028-0836
1476-4687
DOI:10.1038/387049a0