Genetic Analysis of Adipogenesis through Peroxisome Proliferator-activated Receptor γ Isoforms*
By E. Mueller, S. Drori, A. Aiyer, J. Yie, P. Sarraf, Hong Chen, S. Hauser, E. Rosen, Kai Ge, R. Roeder and 1 more. Journal of Biological Chemistry, 2002
236 citations recorded by the source corpus.
Peroxisome proliferator-activated receptor (PPAR) γ is a nuclear receptor that is a key regulator of adipogenesis and is present in two isoforms generated by alternative splicing, PPARγ1 and PPARγ2. Studies of the ability of each isoform to stimulate fat differentiation have yielded ambiguous results, in part because PPARγ stimulates its own expression. We have thus undertaken a formal genetic analysis using PPARγ-null fibroblast cell lines to assess the specific role of each individual isoform in adipogenesis. We show here that both PPARγ1 and PPARγ2 have the intrinsic ability to stimulate robust adipogenesis. Adipose cells stimulated by either PPARγ1 or PPARγ2 express a similar gene profile and show similar responses to insulin. However, in response to low ligand concentrations, PPARγ2 shows a quantitatively greater ability to induce adipogenesis. Analyses involving coactivator binding and transcriptional assays indicate that PPARγ2 has an enhanced ability to bind components of the DRIP/TRAP complex, coactivators required for fat differentiation.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/548f9d4cb8a763512ad35ec5010a82967d0fa546
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In Physiology
Citations in the corpus
- Transcriptional control of adipocyte formation. (2006, background): “Studies performed in pparg2/2 mouse embryonic fibroblasts (MEFs) demonstrate that ectopic PPARg1 is as capable of inducing adipogenesis as PPARg2 (Mueller et al., 2002).”