Takayuki Takahashi

TL;DR: A novel mechanism of anti-inflammatory activity which is based on the direct inhibition and modification of the IKKβ subunit of IKK is demonstrated, which explains how cyclopentenone prostaglandins function and can be used to improve the utility of COX2 inhibitors.

TL;DR: It is proposed that the IKK gamma/NEMO-deficient cells trigger an inflammatory reaction that eventually leads to their death, and this unique self-limiting disease, the first to be genetically linked to the Ikk signaling pathway, is dependent on X-chromosome inactivation.

TL;DR: Overexpression of IKKβ (C179A) protects NF-κB from inhibition by arsenite, indicating that despite the involvement of a large number of distinct gene products in this activation pathway, the critical target for inhibition by arsenic is on the IKK catalytic subunits.

TL;DR: Two transcription factors, NF-κB and AP-1, have emerged in recent years as major targets for signaling pathways that are activated by a variety of proinflammatory stimuli and their regulation by oxidative stress and pro-oxidants will be addressed.

TL;DR: It is demonstrated that hypoestoxide (HE) abrogates the production of pro-inflammatory cytokines (IL-1beta, IL-6, and TNF-alpha) in lipopolysaccharide (LPS)-activated normal human peripheral blood mononuclear cells and inhibition of nitric oxide by IL-1 beta- or IL-17-stimulated normal human chondrocytes.