ArticlePloS one2013
PPARγ regulates expression of carbohydrate sulfotransferase 11 (CHST11/C4ST1), a regulator of LPL cell surface binding.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Genome-Wide Association Studies of Growth and Carcass Traits in Charolais Cattle Based on High-Coverage Whole-Genome Resequencing.International journal of molecular sciences · 2025Article
- Differential Genetic Architecture of Insulin Resistance (HOMA-IR) Based on Obesity Status: Evidence from a Large-Scale GWAS of Koreans.Current issues in molecular biology · 2025Article
- Article
- Unraveling genomic associations with feed efficiency and body weight traits in chickens through an integrative approach.BMC genetics · 2019Article
- Degradation of selenoprotein S and selenoprotein K through PPARγ-mediated ubiquitination is required for adipocyte differentiation.Cell death and differentiation · 2019Article
- Natural helix 9 mutants of PPARγ differently affect its transcriptional activity.Molecular metabolism · 2019Article
- Integration of genome wide association studies and whole genome sequencing provides novel insights into fat deposition in chicken.Scientific reports · 2018Article
- Diet-induced hypercholesterolemia alters liver glycosaminoglycans and associated-lipoprotein receptors in rats.Journal of physiology and biochemistry · 2017Article
- Emerging strategies of targeting lipoprotein lipase for metabolic and cardiovascular diseases.Drug discovery today · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor PPARγ is the key regulator of adipocyte differentiation, function and maintenance, and the cellular target of the insulin-sensitizing thiazolidinediones. Identification and functional characterization of genes regulated by PPARγ will therefore lead to a better understanding of adipocyte biology and may also contribute to the development of new anti-diabetic drugs. Here, we report carbohydrate sulfotransferase 11 (Chst11/C4st1) as a novel PPARγ target gene. Chst11 can sulphate chondroitin, a major glycosaminoglycan involved in development and disease. The Chst11 gene contains two functional intronic PPARγ binding sites, and is up-regulated at the mRNA and protein level during 3T3-L1 adipogenesis. Chst11 knockdown reduced intracellular lipid accumulation in mature adipocytes, which is due to a lowered activity of lipoprotein lipase, which may associate with the adipocyte cell surface through Chst11-mediated sulfation of chondroitin, rather than impaired adipogenesis. Besides directly inducing Lpl expression, PPARγ may therefore control lipid accumulation by elevating the levels of Chst11-mediated proteoglycan sulfation and thereby increasing the binding capacity for Lpl on the adipocyte cell surface.
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