Role of peroxisome proliferator-activated receptors alpha and gamma in gastric ulcer: An overview of experimental evidences

Figure 1 Peroxisome proliferator-activated receptors - mediated mechanisms of transcriptional regulation. In the absence of ligands, peroxisome proliferator-activated receptors (PPARs) bind the promoters of their target genes and repress transcription by recruiting the corepressor complex. In the presence of ligands, PPARs can induce either ligand-dependent transactivation or transrepression. Transactivation involves PPARs heterodimerization with the retinoid X receptors (RXRs) followed by recognition of specific PPAR response elements (PPREs) and interaction with coactivators. Transrepression involves interference with other signal transduction pathways, including NF-κB, STAT, and AP1. NCoR: Nuclear receptor corepressor; NF-κB-RE: NF-κB response element; IFN-RE: Interferon-stimulated gene factor responsive element; TRE-RE: O-tetradecanoylphorbol 13-acetate-responsive element; HDAC: Histone deacetylase; CBP: CREB binding protein; PGC1:Peroxisome proliferator activated receptor gamma coactivator 1; STATs: Signal transducers and activators of transcription.