Learn More
Antirheumatic gold compounds have been shown to inhibit NF-kappaB activation by blocking IkappaB kinase (IKK) activity. To examine the possible inhibitory mechanism of gold compounds, we expressed wild type and mutant forms of IKKalpha and beta subunits in COS-7 cells and determined the effect of gold on the activity of these enzymes both in vivo and in(More)
Interleukin-18 (IL-18) is a novel pro-inflammatory cytokine which has been implicated to play a pathogenic role in rheumatoid arthritis (RA). Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis in rheumatoid synoviocytes. In present study, we examined the effect of IL-18 on VEGF production in fibroblast-like synoviocytes (FLS)(More)
The NF-kappaB/iNOS pathway stimulates muscle differentiation downstream of the PI 3-kinase/p38 MAPK pathway and diverse antioxidants block muscle differentiation. Therefore, we here investigated whether Nox 2 links those two myogenic pathways in H9c2 and C2C12 myoblasts. Compared with the proliferation stage, ROS generation was enhanced from the early stage(More)
Antirheumatic gold compounds have been shown to inhibit NF-κB activation by blocking IκB kinase (IKK) activity. To examine the possible inhibitory mechanism of gold compounds, we expressed wild type and mutant forms of IKKα and β subunits in COS-7 cells and determined the effect of gold on the activity of these enzymes both in vivo and in vitro.(More)
During ischemia-reperfusion injury, brief pre-exposure to oxidative stress renders organs resistant to subsequent severe damage. NF-κB is a transcription factor that is involved in reperfusion-induced inflammatory and immune responses. The activity of NF-κB has been shown to be modulated by oxidative stress in various cell types through different pathways.(More)
Previous work revealed that recurrent mutations (= mutation occurring more than once) in the tandemly repeated arrays present in nontranscribed spacers (NTS) of ribosomal RNA genes (rDNA) are clustered, i.e., they most frequently occur in repeats with adjacent or alternate distribution. A possible explanation is that the likelihood of heteroduplex(More)
There are multiple lines of evidence supporting that chronic inflammation is linked to carcinogenesis. Nuclear factor-kappaB (NF-kappaB), a major redox-sensitive transcription factor responsible for the induction of a wide array of pro-inflammatory genes, is frequently overactivated in many tumors. Moreover, constitutive activation of IkappaB kinase (IKK),(More)
Reactive oxygen species (ROS) has been implicated as an inducer of NF-κB activity in numbers of cell types where exposure of cells to ROS such as H2O2 leads to NF-κB activation. In contrast, exposure to oxidative stress in certain cell types induced reduction of tumor necrosis factor (TNF)-induced NF-κB activation. And various thiol-modifying agents(More)
Aurora-A, a serine/threonine kinase that is overexpressed in certain human cancer cell lines, plays an important role in mitotic progression. Aurora-A has also been reported to be involved in the activation of nuclear factor kappa B (NF-kappaB). The purpose of the present study was to identify the role of Aurora-A in the radiation-induced activation pathway(More)
N-Tosyl-L-phenylalanine chloromethyl ketone (TPCK), a serine/cysteine protease inhibitor, has been reported to inhibit expression of inflammatory mediators by blocking nuclear factor-kappaB (NF-kappaB) activation. We examined the effect of TPCK on the NF-kappaB activation pathway in HeLa cells by measuring the activity of IkappaB kinase (IKK) and(More)