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MINIREVIEW

Activation of Mitogen-Activated Protein Kinases by Peroxisome Proliferator-Activated Receptor Ligands: An Example of Nongenomic Signaling

Curriculum in Toxicology (O.S.G., B.J.D.), and Department of Pharmacology (L.M.G.), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Peroxisome proliferator-activated receptors (PPARs) are a subfamily of nuclear hormone receptors that function as ligand-activated transcription factors to regulate lipid metabolism and homeostasis. In addition to their ability to promote gene transcription in a PPAR-dependent manner, ligands for this receptor family have recently been shown to induce mitogen-activated protein kinase (MAPK) phosphorylation. It is noteworthy that the transcriptional changes induced by PPAR ligands can be separated into distinct PPAR- and MAPK-dependent signaling pathways, suggesting that MAPKs alone mediate some of the effects of PPAR agonists in a nongenomic manner. This review will highlight recent studies that elucidate the nongenomic mechanisms of PPAR ligand-induced MAPK phosphorylation. The potential relevance of MAPK signaling in PPAR biology is also discussed.

Address correspondence to: Lee M. Graves, CB 7365, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599. E-mail: lmg{at}med.unc.edu

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