SUMOylation and PPARgamma: wrestling with inflammatory signaling

Noam Zelcer; Peter Tontonoz

doi:10.1016/j.cmet.2005.10.004

SUMOylation and PPARgamma: wrestling with inflammatory signaling

Cell Metab. 2005 Nov;2(5):273-5. doi: 10.1016/j.cmet.2005.10.004.

Authors

Noam Zelcer¹, Peter Tontonoz

Affiliation

¹ Howard Hughes Medical Institute, Department of Pathology and Laboratory Medicine, University of California, Los Angeles, Los Angeles, California 90055, USA.

PMID: 16271524
DOI: 10.1016/j.cmet.2005.10.004

Abstract

The molecular mechanisms whereby PPARgamma inhibits inflammatory gene expression in macrophages are poorly understood. In a recent Nature paper, provide a new model for trans-repression in which ligand-dependent SUMOylation of PPARgamma results in its recruitment to the promoters of inflammatory genes where it inhibits transcription by preventing clearance of corepressor complexes.

MeSH terms

Animals
Inflammation / genetics*
Inflammation / metabolism
Lipopolysaccharides
Macrophages / drug effects
Macrophages / metabolism
Mice
Multiprotein Complexes / metabolism
Nitric Oxide Synthase Type II / genetics
Nitric Oxide Synthase Type II / metabolism
Nuclear Proteins / biosynthesis
Nuclear Proteins / metabolism*
Nuclear Receptor Co-Repressor 1
PPAR gamma / agonists
PPAR gamma / metabolism*
Promoter Regions, Genetic
Repressor Proteins / biosynthesis
Repressor Proteins / metabolism*
SUMO-1 Protein / metabolism*

Substances

Lipopolysaccharides
Multiprotein Complexes
Ncor1 protein, mouse
Nuclear Proteins
Nuclear Receptor Co-Repressor 1
PPAR gamma
Repressor Proteins
SUMO-1 Protein
Nitric Oxide Synthase Type II