Glucocorticoid receptor directly regulates the transcriptional activity of peroxisome proliferator-activated alpha (PPARα) before birth in anticipation of the sudden shifts in the postnatal nutrient source and metabolic demands.

Curcumin regulates gene expression via PPARa activation and exhibits biological activities involved in amyloidosis, peroxisome proliferation, lipid metabolism, and hepatocyte hypertrophy.

TRIM23 plays a critical role in the switching from early to late adipogenic enhanceosomes by stabilizing the PPARγ protein.

Synthetic PPARγ ligands push and cobind with natural endogenous ligands, instead of compete and displace, which synergistically affects the structure and function of PPARγ.

Dnmt3a and Dnmt3b are dispensable for epidermal homeostasis but act as potent tumor suppressors regarding skin squamous tumorigenesis.

The PPARγ protein acts in macrophages to inhibit breast cancer progression and mediate the anti-tumor effects of rosiglitazone by suppressing Gpr132 – a pro-tumor and pro-inflammatory factor in macrophages.

A systemic hormone controls progenitor fate decisions independent of local fate determining pathways in the adult intestinal stem cell niche of Drosophila melanogaster..

B cell lymphoma 6 (BCL6) represses fasting gene expression by opposing peroxisome proliferator-activated receptor alpha (PPARa) activity at enhancers, and its ablation protects against steatosis by enhancing fatty acid catabolism.

Bladder-cancer-associated RXRA mutations were found to stimulate urothelial proliferation through a mechanism susceptible to small molecule inhibitors of Peroxisome Proliferator-Activated Receptors, credentialing a new class of targetable drivers of bladder cancer.

A combination of cellular, biochemical, genetic and genomic techniques have revealed a new molecular player in the production of fat cells in mice, which could improve our understanding of obesity.