Fig. 3. Schematic of the anti-inflammatory mechanisms of LXR ligands in IFN-γ-stimulated astrocytes (18). IFN-γ triggers an early response in which STAT1 is phosphorylated and translocated to the nucleus, thereby inducing inflammatory gene expression. Synthetic and oxysterol derivatives of LXR ligands trigger the formation of PIAS1 (or HDAC4)-pSTAT1-LXR β (or LXR α) trimers, a process mediated by the differential conjugation of SUMO (Su) to individual LXRs. This blocks the binding of STAT1 to the promoters of its target genes.
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