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. 2018 Apr 3;16:401–413. doi: 10.1016/j.redox.2018.04.001

Fig. 3.

Fig. 3

MsrA deletion abrogates the interaction of Nrf2 with Keap1, resulting in Nrf2 nuclear localization and transcriptional activity. (A, B) Representative immunoblots (A) and quantitation (B) of the interaction of Keap1 with p62 in MsrA-/- and WT VSMC. Immunoprecipitation for Keap1, immunoblots for p62 and Keap1. n = 6 biological replicates. (C, D) Representative immunoblots (C) and quantitation (D) of the interaction of Keap1 with Nrf2. Immunoprecipitation for Nrf2, immunoblots for Keap1 and Nrf2. n = 4 biological replicates. (E-G) Representative immunoblot (E) and summary data for Nrf2 localization in nuclear (F) and cytoplasmic fractions (G) of MsrA-/- and WT VSMC. TOPO IIβ: nuclear marker; GAPDH: cytoplasmic marker. n = 7 biological replicates. (H) Nrf2-dependent transcriptional activity as determined by quantification of ARE-dependent luciferase activity in MsrA-/- and WT VSMC expressing ARE-luciferase reporter. n = 6 biological replicates. * p < 0.05 versus WT by two-tailed t-test.