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Recent advances towards understanding redox mechanisms in the activation of nuclear factor kappaB.
Recent insights are addressed into the NF-kappaB signaling cascades that are triggered by proinflammatory cytokines such as TNF-alpha and IL-1beta and how redox regulation of NF- kappaB activation is likely to involve multiple subcellular compartments. Expand
Redox-based regulation of signal transduction: principles, pitfalls, and promises.
Some of the recent findings that illuminate the significance of redox signaling and exciting future perspectives are reviewed to highlight some of the current pitfalls and the approaches needed to advance this important area of biochemical and biomedical research. Expand
Dynamic redox control of NF-κB through glutaredoxin-regulated S-glutathionylation of inhibitory κB kinase β
The physiological relevance of the S-glutathionylation–GRX redox module in controlling the magnitude of activation of the NF-κB pathway is demonstrated. Expand
Nitric oxide represses inhibitory κB kinase through S-nitrosylation
It is demonstrated here that S-nitrosothiols (SNO) caused a dose-dependent inhibition of the enzymatic activity of IKK, in lung epithelial cells and in Jurkat T cells, which was associated with S- Nitrosylation of the IKK complex, providing an additional mechanism for its antiinflammatory properties. Expand
Tumor necrosis factor‐alpha inhibits myogenic differentiation through MyoD protein destabilization
It is implicate that TNFα inhibits myogenic differentiation through destabilizing MyoD protein in a NF‐κB‐dependent manner, which interferes with skeletal muscle regeneration and may contribute to muscle wasting. Expand
A Prominent Role for Airway Epithelial NF-κB Activation in Lipopolysaccharide-Induced Airway Inflammation1
It is demonstrated that airway epithelial cells play a prominent role in orchestrating the airway inflammatory response to LPS and suggest that NF-κB signaling in these cells is important for modulating innate immune responses to microbial products. Expand
Inflammatory cytokines inhibit myogenic differentiation through activation of nuclear factor-kappaB.
It is demonstrated that inflammatory cytokines may contribute to muscle wasting through the inhibition of myogenic differentiation via a NF-kappaB-dependent pathway. Expand
Recent advances torwards understanding redox mechanisms in the activation of nuclear factor κb
The transcription factor, nuclear factor-kappaB (NF-kappaB) has been studied extensively due to its prominent role in the regulation of immune and inflammatory genes, apoptosis, and cellExpand
Hydrogen Peroxide Signaling through Tumor Necrosis Factor Receptor 1 Leads to Selective Activation of c-Jun N-terminal Kinase*
Binding of tumor necrosis factor-α (TNFα) to its receptor, TNF-R1, results in the activation of inhibitor of κB kinase (IKK) and c-Jun N-terminal kinase (JNK) pathways that are coordinately regulatedExpand
Redox-sensitive kinases of the nuclear factor-kappaB signaling pathway.
The crosstalk of NF-kappaB with other signaling pathways is therefore critical for cellular fate, notably survival or cell death under oxidative conditions, and will also be reviewed. Expand