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. 2021 Feb 8;17(3):834–847. doi: 10.7150/ijbs.57099

Figure 5.

Figure 5

AGR2 acts as a stabilizer for FABP1. A. Huh7 cells were treated with 10 µM CHX for 0, 4, 8 and 12 h. FABP1, ACSL3 and ACSL5 were detected by western blotting. Quantification was performed by normalizing proteins to β-actin. B. Immunofluorescence staining of FABP1 and AGR2 in primary hepatocytes from Agr2/Tg mice. C. In silico prediction of interactions between AGR2 and FABP1. Green, AGR2; blue, FABP1. D. Co-immunoprecipitation analysis of the interaction between AGR2 and FABP1 using Huh7 cell lysates. E. Co-immunoprecipitation analysis of the interaction between AGR2 and FABP1 using cell lysates in HepG2 cells treated with AGR2 and AGR2-C81A expression plasmids. F. His pulldown analysis of the interaction between AGR2 and FABP1. G. His pulldown assays show that the mutation of thioredoxin motif blocks the AGR2-FABP1 interaction. H. His pulldown assays showing the direct interaction of AGR2 and its deletion mutants with FABP1. I. His pulldown assays show that β-ME blocks the AGR2-FABP1 interaction. Representative figures were generated with data from at least three independent experiments. The data are presented as the mean ± SD values. *P < 0.05 by Student's t test.