Fig. 1

Signal transduction of liver X receptors. A Inactive state: LXR-RXR complex binds to corepressors when ligands are absent, and downstream gene transcription is inhibited. B Activation: endogenous or synthetic ligands (L) trigger conformational change of LXR-RXR complex, leading to the release of corepressors and recruitment of coactivators and downstream gene transcription. C Trans-repression: SUMOylated ligand-binding LXR monomer interacts with NFκB, AP-1 and STAT1, inhibiting pro-inflammatory gene transcription. D Cis-repression: ligand-binding LXR monomer conjugates to pro-inflammatory gene enhancers, mediating chromatin closing and inhibiting pro-inflammatory gene transcription. ABCA 1 ATP binding cassette subfamily A member 1, ABCG 1/4/5/8 ATP binding cassette subfamily G member 1/4/5/8, ACSL3 Acyl-CoA synthetase long chain family member 3, AP-1 activator protein 1, ASC2 activating signal cointegrator 2, ELOVL 5 elongation of very long chain fatty acids protein 5, FADS 1/2 fatty acid desaturase 1 and 2, HDAC3 histone deacetylase 3, IDOL inducible degrader of low-density lipoprotein receptor, iNOS inducible nitric oxide synthase, LPCAT3 lysophosphatidylcholine acyltransferase 3, LXRE LXR response element, MCP-1 Monocyte chemoattractant protein-1, MMP-9 matrix metalloproteinase-9, NCoR nuclear receptor corepressor, NF-κB nuclear factor kappa B, RANTES regulated upon activation, normal T cell expressed and presumably secreted, SMRT silencing mediator for retinoid and thyroid receptors, STAT1 signal transducer and activator of transcription 1