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
Cancer biomarkers : section A of Disease markers, 22(3), 575-585 (2018-05-31)
To investigate the impact of Bmi-1-mediated NF-κB pathway on the biological characteristics of CD133+ liver cancer stem cells (LCSCs). Flow cytometry was used to isolate CD133+ LCSC cells from Huh7, Hep3B, SK-hep1, and PLC/PRF-5 cells. CD133+ Huh7 cells were divided
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