JSH-23 has been used as a nuclear factor κB (NF-κB) p65 inhibitor.[1][2][3]
Biochem/physiol Actions
JSH-23 is an inhibitor of NF-kB nuclear translocation.
JSH-23 is an inhibitor of NF-kB nuclear translocation. It inhibits LPS and cytokine-induced nuclear translocation of the p65 subunit of NF-kB as analyzed by EMSA and western blot. The compound displays modest potency (IC50 7.1 uM in RAW 264.7), but has the unique property that it does not affect IkB degradation or recovery. The compound dose dependently inhibits LPS induced expression of cytokines, COX2 and iNOS, and presumably binds to, or interferes with the NLS of p65.
The coordination between cellular differentiation and the mesenchymal/stem transition is essential for both embryo development and neoplasia, suggesting a mechanistic link between these two major processes. In this work we show that miR-127, an embryo-expressing lung miRNA, was prominently induced
Clinical science (London, England : 1979), 130(14), 1257-1268 (2016-04-30)
Transcription factor 4 (TCF-4) was recently identified as a candidate gene for the cause of type 2 diabetes, although the mechanisms have not been fully elucidated. In the present study, we demonstrated that the TCF-4 transgene in macrophages aggravated high-fat diet
Macrophage TCF-4 co-activates p65 to potentiate chronic inflammation and insulin resistance in mice.
Kang X et al.
Clinical Science (London, England : 1979), 130, 1257-1257 (2016)
Serum uric acid is reportedly associated with thrombosis development. However, still unclear is the mechanism of high uric acid in thrombosis with the involvement of let-7c. In an aim to fill this void, we conducted this study by treating mice
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