Anti-inflammatory cyclopentenone prostaglandins are direct inhibitors of IκB kinase
By A. Rossi, P. Kapahi, G. Natoli, Takayuki Takahashi, Yi Chen, M. Karin, M. G. Santoro. Nature, 2000
1,423 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Pharmacology
View Paper: https://www.semanticscholar.org/paper/e6360bdfa01f0f5772341cd0003e605709c6a941
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In Cancer Research
- Sebastian M. B. Nijman
- A. Dirac
- T. Brummelkamp
- René Bernards
- T. Lawrence
- Yumi Yamamoto
- E. Rosen
- M. Karin
In Molecular Biology
- B. Spiegelman
- E. Rosen
- René Bernards
- Sebastian M. B. Nijman
- A. Dirac
- T. Brummelkamp
- B. Kalyanaraman
- T. Lawrence
In Pharmacology
Citations in the corpus
- Cyclooxygenase Isozymes: The Biology of Prostaglandin Synthesis and Inhibition (2004, background): “The cyclopentenone PGs may be antiinflammatory since 15-deoxy-PGJ2 seems to resolve carrageenan-induced pleural inflammation in rats (Gilroy et al., 1999; Kawahito et al., 2000; Rossi et al., 2000).”
- Advances in Our Understanding of Oxylipins Derived from Dietary PUFAs. (2015, positive): “COX oxylipins PGA2 Contributes along with PGE2 to the development of Th1-type immune responses, with PGE2 being more potent in human monocyte–derived dendritic cells (103) Inhibits Ca-stimulated ATPase activity of Walker-256 tumor microsomal membranes (104) Represses insulin-like growth factor I gen”
- Inflammatory processes in Alzheimer's disease. (2007, neutral): “Thus, PPARγ is stimulated best by 9-HODE (hydroxyoctadeca-9Z,11E-dienoic acid, 13-HODE and 15deoxy-Δ12,14-prostaglandin J2 (15dPGJ2, although there is now considerable controversy as to whether 15d-PGJ2 is actually a biologically relevant PPARγ activator or the majority of its action is mediated by ”
- The IKK NF-κB system: a treasure trove for drug development (2004, background): “However, cyPGs can directly inhibit activation of NF-κB pathway by blocking IKK-β activit”
- Mixed messages: modulation of inflammation and immune responses by prostaglandins and thromboxanes. (2001, background): “IKK is responsible for the activation of NF-κB by proinflammatory stimuli, so its inhibition prevents translocation of NF-κB to the nucleus and transcription of NF-κB target genes.”
- Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. (2005, background): “These mechanisms range from the control of prostaglandin E2 and leukotriene B4 production, which may affect signal transduction through I B kinase (28, 29), to direct action on nuclear receptors controlling the production of immune-related factors (30).”
- Anti-inflammatory lipid mediators and insights into the resolution of inflammation (2002, background): “Cyclopentenone prostaglandins have been shown to modify conserved cysteine residues that are found in both the trans -acting DNA-binding proteins of NF-κB and elements of the upstream kinase complex — inhibitor of NF-κB (IκB) kinase (IKK) — that activates NF-κ”