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), and inositol-requiring protein enzyme (IRE)-1, which were similar to the increase in response to TM, an ER stress agonist. Moreover, in the current study, the addition of the ER stress inhibitor 4-PBA blocked the expression of PERK, ATF6, and IRE1
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of the inositol-requiring enzyme 1–X-box-binding protein-1 pathway ( 42 ). In addition, modulations of the HSP pathway have been shown to suppress canonical TGF-β and NF-κB signaling. HSP72 blocks NF-κB activation at multiple aspects, such as by
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protein content was similar between groups ( Fig. 3C ). However, in adipose tissue, IH infusion augmented p-eIF2α protein levels and this was prevented by PBA ( P < 0.05, Fig. 4A ). Inositol requiring 1α (IRE1α) showed a similar profile to p-eIF2α
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