ArticleCell metabolism2006
Non-DNA binding, dominant-negative, human PPARgamma mutations cause lipodystrophic insulin resistance.
Article in Cell metabolism, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
87 citing papers in PubMed, 180 citations in OpenAlex.
- Molecular Dynamics of PPAR Nuclear Receptors: From Ligand Binding to Transcriptional Regulation.Cells · 2026Review
- A simple and robust reporter-based framework for deep functional characterization of PPARγ mutants.Endocrinology · 2026Article
- A Novel PPARG R212W Variant Causes Familial Partial Lipodystrophy Type 3: Clinical Presentation and Functional Characterization.International journal of molecular sciences · 2026Article
- Emerging phenotype: Maturity-onset diabetes of the young type 5 (MODY-5) - mechanisms, clinical spectrum, and unmet needs.Diabetology & metabolic syndrome · 2025Review
- An Alternatively Translated Isoform of PPARG Suggests AF-1 Domain Inhibition as an Insulin Sensitization Target.Diabetes · 2025Article
- Peroxisome proliferator-activated receptor gamma mutation in familial partial lipodystrophy type three: A case report and review of literature.World journal of diabetes · 2024Article
- Involvement of a battery of investigated genes in lipid droplet pathophysiology and associated comorbidities.Adipocyte · 2024Review
- Relationship of Fat Mass Ratio, a Biomarker for Lipodystrophy, With Cardiometabolic Traits.Diabetes · 2024Article
- Familial partial lipodystrophy resulting from loss-of-function PPARγ pathogenic variants: phenotypic, clinical, and genetic features.Frontiers in endocrinology · 2024Review
- Phenotypic Differences Among Familial Partial Lipodystrophy Due toJournal of the Endocrine Society · 2022Article
- Inherited basis of visceral, abdominal subcutaneous and gluteofemoral fat depots.Nature communications · 2022Article
- Familial Partial Lipodystrophy-Literature Review and Report of a Novel Variant inDiagnostics (Basel, Switzerland) · 2022Article
- Expression of the preadipocyte marker ZFP423 is dysregulated between well-differentiated and dedifferentiated liposarcoma.BMC cancer · 2022Article
- Rare coding variants in 35 genes associate with circulating lipid levels-A multi-ancestry analysis of 170,000 exomes.American journal of human genetics · 2022Article
- PPARγ-induced upregulation of subcutaneous fat adiponectin secretion, glyceroneogenesis and BCAA oxidation requires mTORC1 activity.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021Article
- PPARγ and Diabetes: Beyond the Genome and Towards Personalized Medicine.Current diabetes reports · 2021Review
- Blocking PPARγ interaction facilitates Nur77 interdiction of fatty acid uptake and suppresses breast cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Importance of Breast Adipose Tissue in Breast Cancer.International journal of molecular sciences · 2020Review
- PPARγ Transcription Deficiency Exacerbates High-Fat Diet-Induced Adipocyte Hypertrophy and Insulin Resistance in Mice.Frontiers in pharmacology · 2020Article
- Aryl hydrocarbon receptor (AhR) regulates adipocyte differentiation by assembling CRL4B ubiquitin ligase to target PPARγ for proteasomal degradation.The Journal of biological chemistry · 2019Article
27 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
24 authors at 10 institutions in 3 countries.
Funding
Abstract
PPARgamma is essential for adipogenesis and metabolic homeostasis. We describe mutations in the DNA and ligand binding domains of human PPARgamma in lipodystrophic, severe insulin resistance. These receptor mutants lack DNA binding and transcriptional activity but can translocate to the nucleus, interact with PPARgamma coactivators and inhibit coexpressed wild-type receptor. Expression of PPARgamma target genes is markedly attenuated in mutation-containing versus receptor haploinsufficent primary cells, indicating that such dominant-negative inhibition operates in vivo. Our observations suggest that these mutants restrict wild-type PPARgamma action via a non-DNA binding, transcriptional interference mechanism, which may involve sequestration of functionally limiting coactivators.
Indexed as
Identifiers
What OpenQuestion holds
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.