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- W1596098981 abstract "Dehydroxymethylepoxyquinomicin (DHMEQ) is a low-m.w. compound that strongly inhibits NF-κB. DHMEQ directly binds to NF-κB subunits and thereby inhibits their nuclear translocation and DNA binding. In this work, we describe novel mechanisms underlying the suppressive effect of DHMEQ on NF-κB. We found that sustained exposure to DHMEQ blocked TNF-α- and IL-1β-induced TGF-β-activated kinase 1 (TAK1)phosphorylation, a crucial event for NF-κB activation upstream of IκB kinase. This inhibition was mediated by reactive oxygen species (ROS). We also found that DHMEQ caused the unfolded protein response (UPR) through generation of ROS. Alleviation of the UPR by chemical and genetic chaperones partially attenuated the suppressive effect of DHMEQ on NF-κB. The UPR-mediated inhibition of NF-κB occurred downstream of degradation of IκBα and phosphorylation of p65, a subunit of NF-κB. Moreover, this effect was mediated by up-regulation of C/EBPβ caused by the UPR. In addition to its known effect on nuclear translocation of NF-κB, DHMEQ thus interferes with the cytokine-induced NF-κB signaling via generation of ROS at both upstream and downstream of the IκB kinase-IκB level. These multiple mechanisms enable DHMEQ to exert the potent, long-lasting anti-inflammatory/anti-cancer activities that have been reported in a wide range of diseases." @default.
- W1596098981 created "2016-06-24" @default.
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- W1596098981 date "2014-04-01" @default.
- W1596098981 modified "2023-09-27" @default.
- W1596098981 title "Suppression of NF‐κB by dehydroxymethylepoxyquinomicin through reactive oxygen species and unfolded protein response (980.1)" @default.
- W1596098981 doi "https://doi.org/10.1096/fasebj.28.1_supplement.980.1" @default.
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