International Union of Pharmacology. LXI. Peroxisome Proliferator-Activated Receptors

@article{Michalik2006InternationalUO,
  title={International Union of Pharmacology. LXI. Peroxisome Proliferator-Activated Receptors},
  author={Liliane Michalik and Johan Auwerx and Joel P. Berger and Vengalil Krishna Chatterjee and Christopher K. Glass and Frank J. Gonzalez and Paul Andr{\'e} Grimaldi and Takashi Kadowaki and Mitchell A. Lazar and Stephen O’Rahilly and Colin Neil Alexander Palmer and Jorge Plutzky and Janardan K. Reddy and Bruce M Spiegelman and Bart Staels and Walter Wahli},
  journal={Pharmacological Reviews},
  year={2006},
  volume={58},
  pages={726 - 741}
}
The three peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors of the nuclear hormone receptor superfamily. They share a high degree of structural homology with all members of the superfamily, particularly in the DNA-binding domain and ligand- and cofactor-binding domain. Many cellular and systemic roles have been attributed to these receptors, reaching far beyond the stimulation of peroxisome proliferation in rodents after which they were initially… Expand
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TLDR
X-ray crystallography revealed that GW0072 occupied the ligand-binding pocket by using different epitopes than the known PPAR agonists and did not interact with the activation function 2 helix, establishing an approach to the design of PPAR ligands with modified biological activities. Expand
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TLDR
It is now established that the species difference between rodents and humans in response to peroxisome proliferators is due in part to PPAR alpha, and future research directions that should be taken to delineate the mechanisms underlying PPARalpha agonist-induced hepatocarcinogenesis are identified. Expand
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TLDR
It is now established that the species difference between rodents and humans in response to peroxisome proliferators is due in part to PPAR α, and future research directions that should be taken to delineate the mechanisms underlying PPARα agonist-induced hepatocarcinogenesis are identified. Expand
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TLDR
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TLDR
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TLDR
Results indicate that PPARs are differentially activated by naturally occurring eicosanoids and related molecules. Expand
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TLDR
The clinical consequences of PPARgamma polymorphisms in humans, as well as several studies in mice using general or tissue-specific knockout techniques, are reviewed, allowing us to hypothesize a general mechanism of PPargamma action and speculate on future trends in the use of PP ARgamma as a target in the treatment of type II diabetes. Expand
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TLDR
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TLDR
It is suggested that ligand binding may alterPPARγ structure in a ligand type-specific way, resulting in distinct PPARγ-coactivator interactions. Expand
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