Atypical transcriptional regulators and cofactors of PPARgamma.

Détails

ID Serval
serval:BIB_5703C9AF8260
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Atypical transcriptional regulators and cofactors of PPARgamma.
Périodique
International Journal of Obesity
Auteur⸱e⸱s
Miard S., Fajas L.
ISSN
0307-0565 (Print)
ISSN-L
0307-0565
Statut éditorial
Publié
Date de publication
2005
Volume
29 Suppl 1
Pages
S10-S12
Langue
anglais
Résumé
Regulation of peroxisome proliferator-activated receptor gamma (PPARgamma) activity is the result of several events. The first control level is the regulation of the expression of PPARgamma. Examples of this regulation, during adipogenesis, is the transactivation of the PPARgamma promoter by transcription factors of the classical pathway, such as C/EBPs or ADD1/SREBP1, but also newly identified factors, such as E2Fs. When preadipocytes re-enter the cell cycle, PPARgamma expression is induced coincident with an increase in DNA synthesis, suggesting the involvement of the E2F family of cell cycle regulators. E2F1 induces PPARgamma transcription during clonal expansion, whereas E2F4 represses PPARgamma expression during terminal adipocyte differentiation. Hence, E2Fs represent the link between proliferative signaling pathways, triggering clonal expansion, and terminal adipocyte differentiation through regulation of PPARgamma expression. A second regulatory level of PPARgamma action is interaction with cofactors. We will focus our attention on the atypical PPARgamma modulators. We have described an interaction between PPARgamma and the retinoblastoma protein, RB, which is both dependent upon ligand binding by PPARgamma and upon the phosphorylation status of RB. The interaction between PPARgamma and RB decreases the transcriptional activity of PPARgamma through recruitment of the histone deacetylase HDAC3. Inhibition of HDAC activity consequently results in a strong activation of PPARgamma.
Mots-clé
Adipocytes/cytology, Adipose Tissue/metabolism, Cell Cycle Proteins/metabolism, Cell Differentiation, Cell Proliferation, DNA-Binding Proteins/metabolism, E2F Transcription Factors, E2F1 Transcription Factor, E2F4 Transcription Factor, Gene Expression Regulation, Histone Deacetylases/metabolism, Humans, Obesity/metabolism, PPAR gamma/genetics, Retinoblastoma Protein/metabolism, Signal Transduction/physiology, Transcription Factors/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/03/2013 16:04
Dernière modification de la notice
20/08/2019 14:11
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