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. 2015 Dec 15;5:18093. doi: 10.1038/srep18093

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Copyright © 2015, Macmillan Publishers Limited

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In HepG2 cells and the livers of C57BL/6J mice, over-expression of PP4 resulted in elevated phosphorylation level of JNK, whereas down-regulation of PP4 and over-expression of PP4RL restored increased phosphorylation of JNK induced by TNF-α (a). SP600125, a JNK signaling inhibitor, restored the aberrant insulin signaling induced by TNF-α (b). The IRS-1 serine 307 phosphorylation induced by PP4 over-expression was strongly inhibited by SP600125 (c). Data represent means ± S.D. (n = 3 independent experiments in vitro; n = 6 mice in vivo). *P < 0.05 and **P < 0.01 versus control; ^#P < 0.05 and ^##P < 0.01; the 2 groups are as indicated by the line. C, control; T, TNF-α; Con AD, control AD.