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. 2022 Nov 8;44(5):1051–1065. doi: 10.1038/s41401-022-00997-1

Fig. 5. ALM upregulated and activated RXRα, which in turn upregulated CDX2.

Fig. 5

Changes in expression of RXRα in tissues and cells. Immunoblotting bands (a, c) and quantitative data (b, d) of RXRα in kidney tissues and cells of each group. Animal experiments: n = 6; *P < 0.05 vs. db/m group. #P < 0.05 vs. db/db group. Cell experiments: P < 0.05 vs. NG group. ^P < 0.05 vs. HG + DMSO group. e RXRα expression and localization observed by immunofluorescence staining (scale bar, 50 μm). f Autodock Vina software predicts the ligand-protein interaction of ALM with RXRα. h PROMO Database predicted RXRα complementation with the promoter sequence of CDX2. g Transcriptional activity of CDX2 gene increased in RXRα overexpression NRK-52E cells. NRK-52E cells were divided into 4 group transfected with Control or pGL3-rno-CDX2 promoter (pGL3-CDX2 promoter) plasmid, or co-transfected with Vector plasmid and pGL3-CDX2 promoter plasmid, or RXRα overexpression and pGL3-CDX2 promoter plasmid, respectively. n = 3; *P < 0.05 vs. Control group. #P < 0.05 vs. Vector + pGL3-CDX2 promoter group. All cell data are mean ± SD from three independent experiments.