Anti-PPAR gamma / PPARG (Middle Region)

0.5mg/ml if reconstituted with 0.2ml sterile DI water. The peroxisome proliferator-activated receptors (PPARs) are a group of three nuclear receptor isoforms, PPAR gamma, PPAR alpha, and PPAR delta, encoded by different genes. PPARs are ligand-regulated transcription factors that control gene expression by binding to specific response elements (PPREs) within promoters. PPAR gamma is a transcription factor that has a pivotal role in adipocyte differentiation and expression of adipocyte-specific genes. The PPAR gamma1 and gamma2 isoforms result from alternative splicing and have ligand-dependent and -independent activation domains. PPAR gamma is a member of a family of nuclear receptors/ligand-dependent transcription factors, which bind to hormone response elements on target gene promoters. PPAR gamma is abundantly expressed in normal lung tissues, especially in endothelial cells, but that its expression is reduced or absent in the angiogenic plexiform lesions of pulmonary hypertensive lungs and in the vascular lesions of a rat model of severe pulmonary hypertension. And it is concluded that fluid shear stress decreases the expression of PPARgamma in endothelial cells and that loss of PPARgamma expression characterizes an abnormal, proliferating, apoptosis-resistant endothelial cell phenotype. Protein function: Nuclear receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the nuclear receptor binds to DNA specific PPAR response elements (PPRE) and modulates the transcription of its target genes, such as acyl-CoA oxidase. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses. Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of ARNTL/BMAL1 in the blood vessels. [The UniProt Consortium]