ArticleGenetics and molecular biology2011
Regulation of adipogenesis by nuclear receptor PPARγ is modulated by the histone demethylase JMJD2C.
Article in Genetics and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Epigenetic vulnerability in endocrine disruption: bridging mechanisms, models, and environmental inequities.Clinical epigenetics · 2026Review
- The inverse relationship between copy number variation burden and age of onset of metabolic syndrome in Korean middle-aged adults.BMC medical genomics · 2026Article
- Integrated Genomic-Metabolomic Analysis for Tri-Categorical Classification of Type 2 Diabetes Status in the Korean Ansan-Ansung Cohort.International journal of molecular sciences · 2025Article
- Mutation of the histone demethylase Gasc1 causes ASD-like symptoms in mice.Inflammation and regeneration · 2025Article
- An integrative framework to prioritize genes in more than 500 loci associated with body mass index.American journal of human genetics · 2024Article
- The PPARα and PPARγ Epigenetic Landscape in Cancer and Immune and Metabolic Disorders.International journal of molecular sciences · 2021Review
- Effect of ciglitazone on adipogenic transdifferentiation of bovine skeletal muscle satellite cells.Journal of animal science and technology · 2021Article
- Histone demethylase JMJD2B/KDM4B regulates transcriptional program via distinctive epigenetic targets and protein interactors for the maintenance of trophoblast stem cells.Scientific reports · 2021Article
- Control of Adipose Cell Browning and Its Therapeutic Potential.Metabolites · 2020Review
- Histone demethylase KDM4D cooperates with NFIB and MLL1 complex to regulate adipogenic differentiation of C3H10T1/2 mesenchymal stem cells.Scientific reports · 2020Article
- Epigenetic Regulation of Adipogenesis in Development of Metabolic Syndrome.Frontiers in cell and developmental biology · 2020Review
- The Beige Adipocyte as a Therapy for Metabolic Diseases.International journal of molecular sciences · 2019Review
- Epigenetic Regulation of Adipogenic Differentiation by Histone Lysine Demethylation.International journal of molecular sciences · 2019Review
- H3K36 trimethylation mediated by SETD2 regulates the fate of bone marrow mesenchymal stem cells.PLoS biology · 2018Article
- A Large Multiethnic Genome-Wide Association Study of Adult Body Mass Index Identifies Novel Loci.Genetics · 2018Article
- The KDM4A/KDM4C/NF-κB and WDR5 epigenetic cascade regulates the activation of B cells.Nucleic acids research · 2018Article
- The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes.Frontiers in genetics · 2018Article
- Kdm4c is Recruited to Mitotic Chromosomes and Is Relevant for Chromosomal Stability, Cell Migration and Invasion of Triple Negative Breast Cancer Cells.Breast cancer : basic and clinical research · 2018Article
- Role of Histone Demethylases in Cardiomyocytes Induced to Hypertrophy.BioMed research international · 2016Article
- Biology of Beige Adipocyte and Possible Therapy for Type 2 Diabetes and Obesity.International journal of endocrinology · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A potential strategy to combat obesity and its associated complications involves modifying gene expression in adipose cells to reduce lipid accumulation. The nuclear receptor Peroxisome Proliferator-activated receptor gamma (PPARγ) is the master regulator of adipose cell differentiation and its functional activation is currently used as a therapeutic approach for Diabetes Mellitus type 2. However, total activation of PPARγ induces undesirable secondary effects that might be set with a partial activation. A group of proteins that produce histone demethylation has been shown to modify the transcriptional activity of nuclear receptors. Here we describe the repressive action of the jumonji domain containing 2C/lysine demethylase 4 C (JMJD2C/KDM4C) on PPARγ transcriptional activation. JMJD2C significantly reduced the rosiglitazone stimulated PPARγ activation. This effect was mainly observed in experiments performed using the Tudor domains that may interact with histone deacetylase class 1 (HDAC) and this interaction probably reduces the mediated activation of PPARγ. Trichostatin A, a HDAC inhibitor, reduces the repressive effect of JMJD2C. When JMJD2C was over-expressed in 3T3-L1 cells, a reduction of differentiation was observed with the Tudor domain. In summary, we herein describe JMJD2C-mediated reduction of PPARgamma transcriptional activation as well as preadipocyte differentiation. This novel action of JMJD2C might have an important role in new therapeutic approaches to treat obesity and its complications.
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