ArticleHepatology (Baltimore, Md.)2011
Transcription coactivator mediator subunit MED1 is required for the development of fatty liver in the mouse.
Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
- The Mediator Complex: A Regulatory Hub for Transcriptional Activity of Nuclear Receptors.Cells · 2025Review
- Genetically Engineered Mice Unveil In Vivo Roles of the Mediator Complex.International journal of molecular sciences · 2023Review
- Review
- MED12 Regulates Human Adipose-Derived Stem Cell Adipogenesis and Mediator Kinase Subunit Expression in Murine Adipose Depots.Stem cells and development · 2022Article
- TcoFBase: a comprehensive database for decoding the regulatory transcription co-factors in human and mouse.Nucleic acids research · 2022Article
- Identification of the Transcription Co-Factor-Related Gene Signature and Risk Score Model for Osteosarcoma.Frontiers in genetics · 2022Article
- Role of Peroxisome Proliferator-Activated Receptors (PPARs) in Energy Homeostasis of Dairy Animals: Exploiting Their Modulation through Nutrigenomic Interventions.International journal of molecular sciences · 2021Review
- Molecular determinants of MED1 interaction with the DNA bound VDR-RXR heterodimer.Nucleic acids research · 2020Article
- miR‑146a improves hepatic lipid and glucose metabolism by targeting MED1.International journal of molecular medicine · 2020Article
- Intestinal bile acid sequestration improves glucose control by stimulating hepatic miR-182-5p in type 2 diabetes.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Multifaceted functions of macrophages in atherosclerosis.Current opinion in lipidology · 2018Article
- SREBP1c mediates the effect of acetaldehyde on Cidea expression in Alcoholic fatty liver Mice.Scientific reports · 2018Article
- Mediator 1 Is Atherosclerosis Protective by Regulating Macrophage Polarization.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Endocrine-disrupting chemicals and fatty liver disease.Nature reviews. Endocrinology · 2017Review
- Cardiac Med1 deletion promotes early lethality, cardiac remodeling, and transcriptional reprogramming.American journal of physiology. Heart and circulatory physiology · 2017Article
- Selective Tissue Distribution Mediates Tissue-Dependent PPARγ Activation and Insulin Sensitization by INT131, a Selective PPARγ Modulator.Frontiers in pharmacology · 2017Article
- Hepatocyte-specific, PPARγ-regulated mechanisms to promote steatosis in adult mice.The Journal of endocrinology · 2017Article
- Dual Outcomes of Rosiglitazone Treatment on Fatty Liver.The AAPS journal · 2016Article
- Regulation of metabolism by the Mediator complex.Biophysics reports · 2016Article
- [Overexpression of PPARγ induces adipogenic steatosis in mouse primary hepatocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledPeroxisome proliferator-activated receptor-γ (PPARγ), a nuclear receptor, when overexpressed in liver stimulates the induction of adipocyte-specific and lipogenesis-related genes and causes hepatic steatosis. We report here that Mediator 1 (MED1; also known as PBP or TRAP220), a key subunit of the Mediator complex, is required for high-fat diet-induced hepatic steatosis as well as PPARγ-stimulated adipogenic hepatic steatosis. Mediator forms the bridge between transcriptional activators and RNA polymerase II. MED1 interacts with nuclear receptors such as PPARγ and other transcriptional activators. Liver-specific MED1 knockout (MED1(ΔLiv) ) mice, when fed a high-fat (60% kcal fat) diet for up to 4 months failed to develop fatty liver. Similarly, MED1(ΔLiv) mice injected with adenovirus-PPARγ (Ad/PPARγ) by tail vein also did not develop fatty liver, whereas mice with MED1 (MED1(fl/fl) ) fed a high-fat diet or injected with Ad/PPARγ developed severe hepatic steatosis. Gene expression profiling and northern blot analyses of Ad/PPARγ-injected mouse livers showed impaired induction in MED1(ΔLiv) mouse liver of adipogenic markers, such as aP2, adipsin, adiponectin, and lipid droplet-associated genes, including caveolin-1, CideA, S3-12, and others. These adipocyte-specific and lipogenesis-related genes are strongly induced in MED1(fl/fl) mouse liver in response to Ad/PPARγ. Re-expression of MED1 using adenovirally-driven MED1 (Ad/MED1) in MED1(ΔLiv) mouse liver restored PPARγ-stimulated hepatic adipogenic response. These studies also demonstrate that disruption of genes encoding other coactivators such as SRC-1, PRIC285, PRIP, and PIMT had no effect on hepatic adipogenesis induced by PPARγ overexpression.
conclusionWe conclude that transcription coactivator MED1 is required for high-fat diet-induced and PPARγ-stimulated fatty liver development, which suggests that MED1 may be considered a potential therapeutic target for hepatic steatosis. (HEPATOLOGY 2011;).
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