https://www.selleckchem.com/pr....oducts/NVP-ADW742.ht
In vitro, DUSP12 overexpression in endothelial cells ameliorated LPS-induced inflammation, apoptosis, and oxidative stress. DUSP12 silencing in endothelial cells aggravated LPS-induced inflammation, apoptosis, and oxidative stress. Furthermore, we found that DUSP12 directly bound to apoptosis signal-regulating kinase 1 (ASK1) to inhibit Jun N-terminal kinase activation (JNK). A JNK1/2 inhibitor and ASK1 siRNA ameliorated the exacerbating effects of DUSP12 knockdown in vitro. CONCLUSIONS Our data demonstrated that DUSP12 suppressed ML

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