ArticleThe Journal of biological chemistry2009
MED19 and MED26 are synergistic functional targets of the RE1 silencing transcription factor in epigenetic silencing of neuronal gene expression.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 73 citations in OpenAlex.
- Leveraging Shared Genetic Architecture Between Psychiatric and Other Medical Disorders Increases Power and Reveals Novel Psychiatric Risk Loci.medRxiv : the preprint server for health sciences · 2026Article
- The molecular basis of transcription initiation by RNA polymerase II.Nature reviews. Molecular cell biology · 2026Review
- Non-canonical subunit functions in multiprotein complexes: insights from the Mediator complex.Biochemical Society transactions · 2026Review
- The Dynamic Roles of Repressor Element 1-Silencing Transcription Factor (REST): A Double-Edged Sword in Neural Health and Disease.Molecular neurobiology · 2025Review
- Mediator complex subunit MED23 dampens antiviral innate immunity by restricting RIG-I expression.PLoS biology · 2025Article
- REST Is Restless in Neuronal and Non-Neuronal Virus Infections: An In Silico Analysis-Based Perspective.Viruses · 2025Review
- KIF15 promotes human glioblastoma progression under the synergistic transactivation of REST and P300.International journal of biological sciences · 2024Article
- MED19 encodes two unique protein isoforms that confer prostate cancer growth under low androgen through distinct gene expression programs.Scientific reports · 2023Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- Deletion ofJournal of thoracic disease · 2023Article
- Investigating the shared genetic architecture and causal relationship between pain and neuropsychiatric disorders.Human genetics · 2023Article
- The Mediator complex as a master regulator of transcription by RNA polymerase II.Nature reviews. Molecular cell biology · 2022Review
- Transcription Pause and Escape in Neurodevelopmental Disorders.Frontiers in neuroscience · 2022Review
- Roles of the Neuron-Restrictive Silencer Factor in the Pathophysiological Process of the Central Nervous System.Frontiers in cell and developmental biology · 2022Review
- Article
- The role of mediator complex subunit 19 in human diseases.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Review
- Mediator Complex Subunit 19 Promotes the Development of Hepatocellular Carcinoma by Regulating the AKT/mTOR Signaling Pathway.Frontiers in oncology · 2021Article
- Oxidative stress-induced aberrant G9a activation disturbs RE-1-containing neuron-specific genes expression, leading to degeneration in human SH-SY5Y neuroblastoma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Mediator complex subunit Med19 binds directly GATA transcription factors and is required with Med1 for GATA-driven gene regulationThe Journal of biological chemistry · 2020Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A key hub for the orchestration of epigenetic modifications necessary to restrict neuronal gene expression to the nervous system is the RE1 silencing transcription factor (REST; also known as neuron restrictive silencer factor, NRSF). REST suppresses the nonspecific and premature expression of neuronal genes in non-neuronal and neural progenitor cells, respectively, via recruitment of enzymatically diverse corepressors, including G9a histone methyltransferase (HMTase) that catalyzes di-methylation of histone 3-lysine 9 (H3K9me2). Recently, we identified the RNA polymerase II transcriptional Mediator to be an essential link between RE1-bound REST and G9a in epigenetic suppression of neuronal genes in non-neuronal cells. However, the means by which REST recruits Mediator to facilitate G9a-dependent extra-neuronal gene silencing remains to be elucidated. Here, we identify the MED19 and MED26 subunits in Mediator as direct physical and synergistic functional targets of REST. We show that although REST independently binds to both MED19 and MED26 in isolation, combined depletion of both subunits is required to disrupt the association of REST with Mediator. Furthermore, combined, but not individual, depletion of MED19/MED26 impairs REST-directed recruitment to RE1 elements of Mediator and G9a, leading to a reversal of G9a-dependent H3K9me2 and de-repression of REST-target gene expression. Together, these findings identify MED19/MED26 as a probable composite REST interface in Mediator and further clarify the mechanistic basis by which Mediator facilitates REST-imposed epigenetic restrictions on neuronal gene expression.
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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.