Figure 5
From: Computational Prediction and Validation of BAHD1 as a Novel Molecule for UlcerativeColitis
Activation of the IKK/NF-κ B and JNK/AP-1 pathways, but not theERK1/2 and p38 pathways, in siBAHD1-treated Caco-2 cells.
Caco-2 cells were treated with negative control siRNA or BAHD1 siRNA. At 48h, they were exposed to the stimulating mixture (inflammatory mediatorsincluding TNF-α, IFN-γ, IL-1β and LPSdescribed before) for 5 minutes (NC+Mix group, siBAHD1+Mixgroup) or not (NC group, siBAHD1 group). (A) The siBAHD1 group showedstronger activation of key proteins in the NF-κ B (the level ofp-IKK α/β, p-IκBα, p-p65increased) and JNK/AP-1 (phosphorylation level of JNK and c-JUN enhanced)pathways. (B) The phosphorylation level of STAT3 showed the sametrend as in (A). Other MAPK pathways such as P38 and ERK1/2 did notshow a significant difference between the NC and siBAHD1 groups in theinflammatory environment. Representative western blots of cell lysates areshown from at least three independent experiments.
