ArticleThe Journal of biological chemistry2019
The subunit assembly state of the Mediator complex is nutrient-regulated and is dysregulated in a genetic model of insulin resistance and obesity.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- Non-canonical subunit functions in multiprotein complexes: insights from the Mediator complex.Biochemical Society transactions · 2026Review
- Antioxidants and Reactive Oxygen Species: Shaping Human Health and Disease Outcomes.International journal of molecular sciences · 2025Review
- Multi-epitope immunocapture of huntingtin reveals striatum-selective molecular signatures.Molecular systems biology · 2025Article
- Widespread discordance between mRNA expression, protein abundance andbioRxiv : the preprint server for biology · 2025Article
- Genetically Engineered Mice Unveil In Vivo Roles of the Mediator Complex.International journal of molecular sciences · 2023Review
- MED12 Regulates Human Adipose-Derived Stem Cell Adipogenesis and Mediator Kinase Subunit Expression in Murine Adipose Depots.Stem cells and development · 2022Article
- Dietary Regulation of Oxidative Stress in Chronic Metabolic Diseases.Foods (Basel, Switzerland) · 2021Review
- MED1 is a lipogenesis coactivator required for postnatal adipose expansion.Genes & development · 2021Article
- Control of Adipocyte Thermogenesis and Lipogenesis through β3-Adrenergic and Thyroid Hormone Signal Integration.Cell reports · 2020Article
- Mutations in Mediator Complex GenesMolecular syndromology · 2020Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The Mediator complex plays a critical role in the regulation of transcription by linking transcription factors to RNA polymerase II. By examining mouse livers, we have found that in the fasted state, the Mediator complex exists primarily as an approximately 1.2-MDa complex, consistent with the size of the large Mediator complex, whereas following feeding, it converts to an approximately 600-kDa complex, consistent with the size of the core Mediator complex. This dynamic change is due to the dissociation and degradation of the kinase module that includes the MED13, MED12, cyclin-dependent kinase 8 (CDK8), and cyclin C (CCNC) subunits. The dissociation and degradation of the kinase module are dependent upon nutrient activation of mTORC1 that is necessary for the induction of lipogenic gene expression because pharmacological or genetic inhibition of mTORC1 in the fed state restores the kinase module. The degradation but not dissociation of the kinase module depends upon the E3 ligase, SCF
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Registered trials
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