PPARα Polyclonal Antibody

Peroxisome proliferator-activated receptor α (PPARα) is a member of the nuclear receptor family of ligand-activated transcription factors that regulates a variety of metabolic functions and inflammation.¹ It contains an N-terminal domain that is subject to phosphorylation, a DNA-binding domain, and a C-terminal ligand-binding domain (Item No. 10009088).² PPARα is highly expressed in tissues with high fatty acid oxidation rates, including the liver, heart, skeletal muscle, brown adipose tissue, and kidney, as well as in macrophages and T cells.^3,2 It is activated by a variety of endogenous ligands such as fatty acids, eicosanoids, and endocannabinoids, as well as synthetic agents, including fenofibrate (Item No. 10005368) and gemfibrozil (Item No. 14835).⁴ Upon activation, PPARα heterodimerizes with the retinoid X receptor (RXR) and binds to PPAR response elements in PPARα target genes, recruiting RNA polymerase II and initiating gene transcription.¹ PPARα transcriptionally regulates a variety of genes involved in several cellular processes, including lipid and hormone transport, peroxisomal and mitochondrial β-oxidation, amino acid metabolism, and inflammation.^1,2 Genome-wide deletion of Ppara protects mice from high-fat diet-induced hyperinsulinemia and insulin resistance.⁵ PPARA SNPs have been found in individuals with a variety of cardiovascular conditions, including hypertension, atherosclerosis, coronary artery disease, left ventricular hypertrophy, or myocardial infarction.¹ Formulations containing PPARα agonists have been used in the treatment of hyperlipidemia. Cayman's PPARα Polyclonal Antibody can be used for immunohistochemistry (IHC) and Western blot (WB) applications. The antibody recognizes the N-terminal region of PPARα at approximately 52 kDa from human, baboon, mouse, and pig samples.

WARNING This product is not for human or veterinary use.

1. Li, S., Yang, B., Du, Y., et al. Targeting PPARα for the treatment and understanding of cardiovascular diseases. Cell Physiol. Biochem. 51(6), 2760-2775 (2018).

2. Pawlak, M., Lefebvre, P., and Staels, B. Molecular mechanism of PPARa action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease. J. Hepatol. 62, 720-733 (2015).

3. Rakhshandehroo, M., Knoch, B., Müller, M., et al. Peroxisome proliferator-activated receptor alpha target genes. PPAR Res. 612089 (2010).

4. Ruscica, M., Busnelli, M., Runfola, E., et al. Impact of PPAR-Alpha polymorphisms-the case of metabolic disorders and atherosclerosis. Int. J. Mol. Sci. 20(18), 4378 (2019).

5. Guerre-Millo, M., Rouault, C., Poulain, P., et al. PPAR-α-null mice are protected from high-fat diet-induced insulin resistance. Diabetes 50(12), 2809-2814 (2001).

Schaedlich, K., Gebauer, S., Hunger, L., et al. DEHP deregulates adipokine levels and impairs fatty acid storage in human SGBS-adipocytes. Sci. Rep. 8(1), 3447 (2018).

Chavan, R., Preitner, N., Okabe, T., et al. REV-ERBa regulated Fgf21 expression in the liver via hepatic nuclear factor 6. Biol. Open 6, 1-7 (2017).

Tzeng, J., Byun, J., Park, J.Y., et al. An ideal PPAR response element bound to and activated by PPARa. PLoS One 10(8), e0134996 (2015).