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.

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

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

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.

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

Par-complex-dependent cell polarity can be cell-autonomously conferred to non-polar Drosophila S2 cells, unveiling temporal patterns toward the cortical localization of Par-complex aggregates that include a meshwork containing unit segments.

Even though the ctenophore Mnemiopsis leidyi develops polarized epithelial tissues, polarization is not mediated by the conserved mechanisms polarizing bilaterian and cnidarian epithelial cells.

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.