ArticleMolecular and cellular biology1996
SIN3-dependent transcriptional repression by interaction with the Mad1 DNA-binding protein.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 59 citations in OpenAlex.
- Analysis of the chromatin landscape and RNA polymerase II binding at SIN3-regulated genes.Biology open · 2023Article
- Systematic identification and characterization of repressive domains in Drosophila transcription factors.The EMBO journal · 2023Article
- Histone Deacetylases with Antagonistic Roles in Saccharomyces cerevisiae Heterochromatin Formation.Genetics · 2016Article
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- Regulation of the yeast Ace2 transcription factor during the cell cycle.The Journal of biological chemistry · 2008Article
- Chromatin-associated genes protect the yeast genome from Ty1 insertional mutagenesis.Genetics · 2008Article
- The mSin3A chromatin-modifying complex is essential for embryogenesis and T-cell development.Molecular and cellular biology · 2005Article
- Sin3: a flexible regulator of global gene expression and genome stability.Current genetics · 2005Review
- Functional analysis of the Mad1-mSin3A repressor-corepressor interaction reveals determinants of specificity, affinity, and transcriptional response.Molecular and cellular biology · 2004Article
- The highly conserved region of the co-repressor Sin3A functionally interacts with the co-repressor Alien.Nucleic acids research · 2004Article
- CHD5, a new member of the chromodomain gene family, is preferentially expressed in the nervous system.Oncogene · 2003Article
- S-phase-specific expression of the Mad3 gene in proliferating and differentiating cells.The Biochemical journal · 2001Article
- Identification of the Sin3-binding site in Ume6 defines a two-step process for conversion of Ume6 from a transcriptional repressor to an activator in yeast.Molecular and cellular biology · 2001Article
- Mlx, a new Max-like bHLHZip family member: the center stage of a novel transcription factors regulatory pathway?Oncogene · 2000Article
- Roles for the Saccharomyces cerevisiae SDS3, CBK1 and HYM1 genes in transcriptional repression by SIN3.Genetics · 2000Article
- Cell type-dependent transactivation or repression of mesoderm-restricted basic helix-loop-helix protein, POD-1/Capsulin.Molecular and cellular biochemistry · 2000Article
- Functional analysis of the SIN3-histone deacetylase RPD3-RbAp48-histone H4 connection in the Xenopus oocyte.Molecular and cellular biology · 1999Article
- Repression by Ikaros and Aiolos is mediated through histone deacetylase complexes.The EMBO journal · 1999Article
- Residues in the Swi5 zinc finger protein that mediate cooperative DNA binding with the Pho2 homeodomain protein.Molecular and cellular biology · 1998Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The SIN3 gene in Saccharomyces cerevisiae encodes a negative regulator of transcription of a large number of genes. Mouse homologs of SIN3 have been identified through screens for proteins interacting with the mammalian Mad1 protein, a transcriptional repressor. We find that yeast Sin3 (ySin3) interacts with Madl and that, as for mouse Sin3, the N terminus of Mad1 interacts with the PAH2 domain of ySin3. Although Mad1 (a basic helix-loop-helix leucine zipper [bHLH-Zip) protein) forms a heterodimer with the Max bHLH-Zip protein, LexA-Mad1 and VP16-Max do not activate transcription of a reporter gene in a two-hybrid assay. This failure in activation is due to direct repression by ySin3, as LexA-Mad1 and VP16-Max are able to activate the two-hybrid reporter in a sin3 mutant. This inhibition of activation by LexA-Mad1 and VP16-Max requires the PAH2 domain of ySin3 and the N-terminal interaction region of Mad1. These data demonstrate that ySin3 functions as a transcriptional repressor by being brought to promoters by interacting with proteins bound to DNA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.