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. 2018 Mar 9;15(5):4213–4222. doi: 10.3892/etm.2018.5944

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Copyright: © Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Endoplasmic reticulum stress and redox homeostasis in vivo. Total proteins were isolated from myocardial tissues and subjected to western blotting. β-actin served as an internal control. (A) Analyses of GRP78 and CHOP. (B) Analyses of Ero1α, Ero1β and PDI. Values are presented as the mean ± standard deviation. *P<0.05 and **P<0.01, as indicated. GRP78, glucose-regulated protein 78; CHOP, CCAAT/enhancer binding protein-homologous protein; Ero1, endoplasmic reticulum oxidoreductase 1; PDI, protein disulfide isomerase; MI, myocardial infarction.