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. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Hepatology. 2016 Aug 23;64(5):1559–1576. doi: 10.1002/hep.28747

Figure 4. NgBR deficiency promotes LXRα nuclear translocation and activates LXRα pathway.

Figure 4

(A) Protein levels of LXRα in total cellular, cytosolic and nuclear extracts of shNSi and shNgBRi cells were determined by western blotting. (B) NgBR deficiency promotes the nuclear translocation of LXRα. Localization of LXRα in shNSi cells, shNgBRi cells, and shNgBRi cells transfected with the plasmid DNA of NgBR-HA were determined by immunofluorescent staining. (C) Total, cytosolic and nuclear proteins were extracted from liver tissue samples of littermate control and NgBR LivKO female mice (n=4). Expression of LXRα was determined by western blotring. (D, E) Localization of LXRα in the frozen liver sections of littermate control and NgBR LivKO female mice was determined by immunofluorescent (D) and immunohistochemical (E) staining. (F) LXR activation increases lipid accumulation. HepG2 cells were treated with LXR ligand (GW3965, 10 μM) for 24 h followed by determination of cellular lipid contents with Oil Red O staining and quantitative analysis. *: P<0.05 vs. control (n=3).