The role of the amino-terminal domain in the interaction of unliganded peroxisome proliferator-activated receptor gamma-2 with nuclear receptor co-repressor.

@article{Suzuki2010TheRO,
  title={The role of the amino-terminal domain in the interaction of unliganded peroxisome proliferator-activated receptor gamma-2 with nuclear receptor co-repressor.},
  author={Sadako Suzuki and Shigekazu Sasaki and Hiroshi Morita and Yutaka Oki and Daisuke Turiya and Takeshi Ito and Hiroko Misawa and Keiko Ishizuka and Hirotoshi Nakamura},
  journal={Journal of molecular endocrinology},
  year={2010},
  volume={45 3},
  pages={
          133-45
        }
}
Peroxisome proliferator-activated receptor gamma-2 (PPARG2) is a ligand-dependent transcriptional factor involved in the pathogenesis of insulin resistance. In the presence of a ligand, PPARG2 associates with co-activators, while it recruits co-repressors (CoRs) in the absence of a ligand. It has been reported that the interaction of liganded PPARG2 with co-activators is regulated by the amino-terminal A/B domain (NTD) via inter-domain communication. However, the role of the NTD is unknown in… 
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References

SHOWING 1-10 OF 94 REFERENCES
p300 interacts with the N- and C-terminal part of PPARgamma2 in a ligand-independent and -dependent manner, respectively.
TLDR
It is shown here that the interaction between p300/CBP and PPARgamma is complex and involves multiple domains in each protein, which could enhance the transcriptional activities of both the activating function (AF)-1 and AF-2 domains.
Ligand-independent activation domain in the N terminus of peroxisome proliferator-activated receptor gamma (PPARgamma). Differential activity of PPARgamma1 and -2 isoforms and influence of insulin.
TLDR
It is demonstrated that PPARgamma has an N-terminal (ligand-independent) activation domain, and that insulin can potentiate the activity of the N-Terminal domain of PPARGamma.
Regulation of the Transcriptional Activity of the Peroxisome Proliferator-activated Receptor α by Phosphorylation of a Ligand-independent trans-Activating Domain*
TLDR
It is demonstrated that amino acids 1–92 of hPPARα contain an activation function (AF)-1-like domain, which is further activated by insulin through a pathway involving the mitogen-activated protein kinases p42 and p44, and the effect of insulin on the AF-1 region of PPARα can be mimicked by the addition of triiodothyronine receptor β1, a strong binder of corepressor proteins.
Inhibitory effect of a proline-to-alanine substitution at codon 12 of peroxisome proliferator-activated receptor-gamma 2 on thiazolidinedione-induced adipogenesis.
TLDR
The results suggest that the P12A substitution in PPARgamma gene may be associated with abnormalities of adipose tissue formation and insulin sensitivity.
T0070907, a Selective Ligand for Peroxisome Proliferator-activated Receptor γ, Functions as an Antagonist of Biochemical and Cellular Activities*
TLDR
Results suggest that the activity of PPARγ antagonists can be modulated by the availability and concentration of RXR agonists.
Nuclear receptor corepressor-dependent repression of peroxisome-proliferator-activated receptor delta-mediated transactivation.
TLDR
The results suggest that the transactivation potential of liganded PPAR delta can be fine-tuned by interaction with NCoR and SMRT in a manner determined by the expression levels of corepressors and coactivators.
The peroxisome proliferator-activated receptor δ, an integrator of transcriptional repression and nuclear receptor signaling
  • Yanhong Shi, M. Hon, R. Evans
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 2002
TLDR
A role for PPARδ as a gateway receptor whose relative levels of expression can be used to modulate PPARα and PPARγ activity is suggested.
A dominant-negative peroxisome proliferator-activated receptor gamma (PPARgamma) mutant is a constitutive repressor and inhibits PPARgamma-mediated adipogenesis.
TLDR
When expressed in primary human preadipocytes using a recombinant adenovirus, this PPARgamma mutant blocks thiazolidinedione-induced differentiation, providing direct evidence that PPargamma mediates adipogenesis.
Peroxisome Proliferator-activated Receptor Mediates Cross-talk with Thyroid Hormone Receptor by Competition for Retinoid X Receptor
TLDR
It is demonstrated that PPAR selectively inhibits the transcriptional activity of TRs by competition for RXR and possibly non-RXR TR-auxiliary proteins, independent of the formation of PPAR:TR heterodimers or competition for DNA binding.
A Dominant-negative Peroxisome Proliferator-activated Receptor γ (PPARγ) Mutant Is a Constitutive Repressor and Inhibits PPARγ-mediated Adipogenesis*
TLDR
When expressed in primary human preadipocytes using a recombinant adenovirus, this PPARγ mutant blocks thiazolidinedione-induced differentiation, providing direct evidence that PParγ mediates adipogenesis.
...
1
2
3
4
5
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