ArticleThe Journal of biological chemistry2013
The Med1 subunit of the mediator complex induces liver cell proliferation and is phosphorylated by AMP kinase.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Crosstalk BetweenCancers · 2026Review
- Deciphering per- and polyfluoroalkyl substances mode of action: comparative gene expression analysis in human liver spheroids.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Mediator complex subunit 1 promotes oral squamous cell carcinoma progression by activating MMP9 transcription and suppressing CD8Journal of experimental & clinical cancer research : CR · 2024Article
- Genome-Wide Association Study Reveals Novel Candidate Genes Influencing Semen Traits in Landrace Pigs.Animals : an open access journal from MDPI · 2024Article
- Med1 inhibits ferroptosis and alleviates liver injury in acute liver failure via Nrf2 activation.Cell & bioscience · 2024Article
- NetREX-CF integrates incomplete transcription factor data with gene expression to reconstruct gene regulatory networks.Communications biology · 2022Article
- MED1 Ablation Promotes Oral Mucosal Wound Healing via JNK Signaling Pathway.International journal of molecular sciences · 2022Article
- Mediator complex subunit 8 is a prognostic biomarker in hepatocellular carcinoma.American journal of translational research · 2022Article
- Mixed Lineage Kinase 3 phosphorylates prolyl-isomerase PIN1 and potentiates GLI1 signaling in pancreatic cancer development.Cancer letters · 2021Article
- Bothrops Jararaca Snake Venom Modulates Key Cancer-Related Proteins in Breast Tumor Cell Lines.Toxins · 2021Article
- Hsa-miR-637 inhibits human hepatocyte proliferation by targeting Med1-interacting proteins.Liver research (Beijing, China) · 2021Article
- Gene Expression Profiles Induced by a Novel Selective Peroxisome Proliferator-Activated Receptor α Modulator (SPPARMα) Pemafibrate.International journal of molecular sciences · 2019Review
- 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
- 2-[2-(4-(trifluoromethyl)phenylamino)thiazol-4-yl]acetic acid (Activator-3) is a potent activator of AMPK.Scientific reports · 2018Article
- Chromatin recruitment of activated AMPK drives fasting response genes co-controlled by GR and PPARα.Nucleic acids research · 2016Article
- Cardiomyocyte-Specific Ablation of Med1 Subunit of the Mediator Complex Causes Lethal Dilated Cardiomyopathy in Mice.PloS one · 2016Article
- PPARα-Deficient ob/ob Obese Mice Become More Obese and Manifest Severe Hepatic Steatosis Due to Decreased Fatty Acid Oxidation.The American journal of pathology · 2015Article
- Epigenetic modification of histone 3 lysine 27: mediator subunit MED25 is required for the dissociation of polycomb repressive complex 2 from the promoter of cytochrome P450 2C9.The Journal of biological chemistry · 2015Article
- MED1 mediates androgen receptor splice variant induced gene expression in the absence of ligand.Oncotarget · 2015Article
- Med1 subunit of the mediator complex in nuclear receptor-regulated energy metabolism, liver regeneration, and hepatocarcinogenesis.Gene expression · 2014Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Mediator, a large multisubunit protein complex, plays a pivotal role in gene transcription by linking gene-specific transcription factors with the preinitiation complex and RNA polymerase II. In the liver, the key subunit of the Mediator complex, Med1, interacts with several nuclear receptors and transcription factors to direct gene-specific transcription. Conditional knock-out of Med1 in the liver showed that hepatocytes lacking Med1 did not regenerate following either partial hepatectomy or treatment with certain nuclear receptor activators and failed to give rise to tumors when challenged with carcinogens. We now report that the adenovirally driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control, and liver-specific genes, indicating that Med1 alone is necessary and sufficient for liver cell proliferation. Importantly, we demonstrate that AMP-activated protein kinase (AMPK), an important cellular energy sensor, interacts with, and directly phosphorylates, Med1 in vitro at serine 656, serine 756, and serine 796. AMPK also phosphorylates Med1 in vivo in mouse liver and in cultured primary hepatocytes and HEK293 and HeLa cells. In addition, we demonstrate that PPARα activators increase AMPK-mediated Med1 phosphorylation in vivo. Inhibition of AMPK by compound C decreased hepatocyte proliferation induced by Med1 and also by the PPARα activators fenofibrate and Wy-14,643. Co-treatment with compound C attenuated PPARα activator-inducible fatty acid β-oxidation in liver. Our results suggest that Med1 phosphorylation by its association with AMPK regulates liver cell proliferation and fatty acid oxidation, most likely as a downstream effector of PPARα and AMPK.
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