Summon SUMO to Wrestle with Inflammation Bin Liu, Ke Shuai  Molecular Cell  Volume 35, Issue 6, Pages 731-732 (September 2009) DOI: 10.1016/j.molcel.2009.09.002 Copyright © 2009 Elsevier Inc. Terms and Conditions

Figure 1 Ligand-Induced SUMOylation of Nuclear Receptors Inhibits NF-κB and STAT1-Mediated Inflammatory Gene Activation Upon ligand stimulation, PIAS1 promotes the conjugation of SUMO1 to PPARγ, and HDAC4 promotes the conjugation of SUMO2 to LXRα or LXRβ. The SUMOylated PPARγ and LXRs then bind to the nuclear receptor corepressor (NCoR)-histone deacetylase (HDAC)-3 complexes on inflammatory gene promoters, resulting in the stabilization of NCoR-HDAC3 complexes and, thus, the inhibition of NF-κB-mediated inflammatory gene induction. In brain astrocytes, ligand stimulation induces HDAC4-mediated SUMO2 conjugation to LXRα and PIAS1-mediated SUMO1 conjugation to LXRβ. The formation of LXRα-HDAC4-STAT1 and LXRβ-PIAS1-STAT1 trimeric complexes prevents the binding of STAT1 to gene promoters, resulting in the inhibition of IFN-γ-induced inflammatory gene activation. Su1, SUMO1; Su2, SUMO2; filled circle, NR ligand. Molecular Cell 2009 35, 731-732DOI: (10.1016/j.molcel.2009.09.002) Copyright © 2009 Elsevier Inc. Terms and Conditions