ArticleProceedings of the National Academy of Sciences of the United States of America1999
Neural restrictive silencer factor recruits mSin3 and histone deacetylase complex to repress neuron-specific target genes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 232 citations in OpenAlex.
- Pioneer factor ETV2 safeguards endothelial cell specification by recruiting the repressor REST to restrict alternative lineage commitment.Nature cardiovascular research · 2025Article
- Sleep and diurnal alternative polyadenylation sites associated with human APA-linked brain disorders.Research square · 2024Article
- Sleep and diurnal alternative polyadenylation sites associated with human APA-linked brain disorders.Npj biological timing and sleep · 2024Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- REST in the Road Map of Brain Development.Cellular and molecular neurobiology · 2023Review
- Cholinergic regulation of vascular endothelial function by human ChATProceedings of the National Academy of Sciences of the United States of America · 2023Article
- MYT1L is required for suppressing earlier neuronal development programs in the adult mouse brain.Genome research · 2023Article
- How AlphaFold2 Predicts Conditionally Folding Regions Annotated in an Intrinsically Disordered Protein Database, IDEAL.Biology · 2023Article
- Roles of the Neuron-Restrictive Silencer Factor in the Pathophysiological Process of the Central Nervous System.Frontiers in cell and developmental biology · 2022Review
- Knockdown of NRSF Alleviates Ischemic Brain Injury and Microvasculature Defects in Diabetic MCAO Mice.Frontiers in neurology · 2022Article
- The functions of repressor element 1-silencing transcription factor in models of epileptogenesis and post-ischemia.Metabolic brain disease · 2021Review
- Multifaceted effect of chlorpromazine in cancer: implications for cancer treatment.Oncotarget · 2021Article
- Mechanism of REST/NRSF regulation of clustered protocadherin α genes.Nucleic acids research · 2021Article
- Difference of binding modes among three ligands to a receptor mSin3B corresponding to their inhibitory activities.Scientific reports · 2021Article
- Transcriptional regulation of adult neural stem/progenitor cells: tales from the subventricular zone.Neural regeneration research · 2020Review
- Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020Review
- The neuronal transcription factor Myt1L interacts via a conserved motif with the PAH1 domain of Sin3 to recruit the Sin3L/Rpd3L histone deacetylase complex.FEBS letters · 2020Article
- The transcription factor REST up-regulates tyrosine hydroxylase and antiapoptotic genes and protects dopaminergic neurons against manganese toxicity.The Journal of biological chemistry · 2020Article
- RE1-silencing transcription factor controls the acute-to-chronic neuropathic pain transition andThe Journal of biological chemistry · 2018Article
- Sertraline, chlorprothixene, and chlorpromazine characteristically interact with the REST-binding site of the corepressor mSin3, showing medulloblastoma cell growth inhibitory activities.Scientific reports · 2018Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulative evidence suggests that more than 20 neuron-specific genes are regulated by a transcriptional cis-regulatory element known as the neural restrictive silencer (NRS). A trans-acting repressor that binds the NRS, NRSF [also designated RE1-silencing transcription factor (REST)] has been cloned, but the mechanism by which it represses transcription is unknown. Here we show evidence that NRSF represses transcription of its target genes by recruiting mSin3 and histone deacetylase. Transfection experiments using a series of NRSF deletion constructs revealed the presence of two repression domains, RD-1 and RD-2, within the N- and C-terminal regions, respectively. A yeast two-hybrid screen using the RD-1 region as a bait identified a short form of mSin3B. In vitro pull-down assays and in vivo immunoprecipitation-Western analyses revealed a specific interaction between NRSF-RD1 and mSin3 PAH1-PAH2 domains. Furthermore, NRSF and mSin3 formed a complex with histone deacetylase 1, suggesting that NRSF-mediated repression involves histone deacetylation. When the deacetylation of histones was inhibited by tricostatin A in non-neuronal cells, mRNAs encoding several neuronal-specific genes such as SCG10, NMDAR1, and choline acetyltransferase became detectable. These results indicate that NRSF recruits mSin3 and histone deacetylase 1 to silence neural-specific genes and suggest further that repression of histone deacetylation is crucial for transcriptional activation of neural-specific genes during neuronal terminal differentiation.
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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.