ArticleGenes & development2014
Anti-diabetic rosiglitazone remodels the adipocyte transcriptome by redistributing transcription to PPARγ-driven enhancers.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 105 citations in OpenAlex.
- Mendelian randomization facilitates identification of schizophrenia risk enhancer RNAs.Molecular psychiatry · 2026Article
- Multimodal epigenetic and enhancer network remodeling shape the transcriptional landscape of human beige adipocytes.Communications biology · 2026Article
- MicroRNA gene dynamics in immune cell subpopulations during aging and atherosclerosis disease development at single-cell resolution.Genome medicine · 2025Article
- Agonists of the Nuclear Receptor PPARγ Can Produce Biased Signaling.Molecular pharmacology · 2024Article
- Short-term cold exposure induces persistent epigenomic memory in brown fat.Cell metabolism · 2024Article
- NKX2-2 based nuclei sorting on frozen human archival pancreas enables the enrichment of islet endocrine populations for single-nucleus RNA sequencing.BMC genomics · 2024Article
- Alternative isoform expression of key thermogenic genes in human beige adipocytes.Frontiers in endocrinology · 2024Article
- PPARγ lipodystrophy mutants reveal intermolecular interactions required for enhancer activation.Nature communications · 2022Article
- Transcriptional control of energy metabolism by nuclear receptors.Nature reviews. Molecular cell biology · 2022Review
- Enhancer RNA (eRNA) in Human Diseases.International journal of molecular sciences · 2022Review
- Transcriptomic profiling of the telomerase transformed Mesenchymal stromal cells derived adipocytes in response to rosiglitazone.BMC genomic data · 2022Article
- Isoform-specific functions of PPARγ in gene regulation and metabolism.Genes & development · 2022Article
- Integrative analysis reveals multiple modes of LXR transcriptional regulation in liver.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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- A coregulator shift, rather than the canonical switch, underlies thyroid hormone action in the liver.Genes & development · 2021Article
- Using GRO-Seq to Measure Circadian Transcription and Discover Circadian Enhancers.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Curated gene expression dataset of differentiating 3T3-L1 adipocytes under pharmacological and genetic perturbations.Adipocyte · 2020Article
- Molecular determinants of MED1 interaction with the DNA bound VDR-RXR heterodimer.Nucleic acids research · 2020Article
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- WWP1 knockout in mice exacerbates obesity-related phenotypes in white adipose tissue but improves whole-body glucose metabolism.FEBS open bio · 2020Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Rosiglitazone (rosi) is a powerful insulin sensitizer, but serious toxicities have curtailed its widespread clinical use. Rosi functions as a high-affinity ligand for peroxisome proliferator-activated receptor γ (PPARγ), the adipocyte-predominant nuclear receptor (NR). The classic model, involving binding of ligand to the NR on DNA, explains positive regulation of gene expression, but ligand-dependent repression is not well understood. We addressed this issue by studying the direct effects of rosi on gene transcription using global run-on sequencing (GRO-seq). Rosi-induced changes in gene body transcription were pronounced after 10 min and correlated with steady-state mRNA levels as well as with transcription at nearby enhancers (enhancer RNAs [eRNAs]). Up-regulated eRNAs occurred almost exclusively at PPARγ-binding sites, to which rosi treatment recruited coactivators, including MED1, p300, and CBP. In contrast, transcriptional repression by rosi involved a loss of coactivators from eRNA sites devoid of PPARγ and enriched for other transcription factors, including AP-1 factors and C/EBPs. Thus, rosi activates and represses transcription by fundamentally different mechanisms that could inform the future development of anti-diabetic drugs.
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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.