2010
DOI: 10.4049/jimmunol.0903131
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Inhibitor of NF-κB Kinases α and β Are Both Essential for High Mobility Group Box 1-Mediated Chemotaxis

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Cited by 89 publications
(111 citation statements)
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“…17 Phosphorylation of IKK is essential for inflammation triggering macrophage chemotaxis. 19 As already shown in other cell types, 21,22 SGK1 effectively regulates transcription by upregulating NF-κB activity through phosphorylation and activation of IKKα/β. Thus, SGK1 enhances the ability of IKKα/β to phosphorylate endogenous IκBα.…”
Section: Discussionmentioning
confidence: 85%
See 1 more Smart Citation
“…17 Phosphorylation of IKK is essential for inflammation triggering macrophage chemotaxis. 19 As already shown in other cell types, 21,22 SGK1 effectively regulates transcription by upregulating NF-κB activity through phosphorylation and activation of IKKα/β. Thus, SGK1 enhances the ability of IKKα/β to phosphorylate endogenous IκBα.…”
Section: Discussionmentioning
confidence: 85%
“…9,18 The proinflammatory transcription factor NF-κB is retained inactive in the cytoplasm through association with the inhibitor κB (IκB) protein. 19 On phosphorylation, IκB kinase (IKK) phosphorylates IκB thus initiating the ubiquitination and subsequent degradation of IκB followed by translocation of NF-κB into the nucleus with initiation of NF-κB-dependent gene expression. 2,20 Atherogenesis requires multiple cell signaling mechanisms involving different protein kinases such as phosphoinositide-3 kinase (PI3K).…”
mentioning
confidence: 99%
“…Nilvadipine has been shown to inhibit nuclear factor-κB (NFκB)-dependent transcription (38) and, as expected for an NFκB inhibitor, nilvadipine users have reduced plasma cytokine levels (39). Interestingly, both RAGE and BACE-1 expression are regulated by NFκB (40)(41)(42)(43). In particular, inhibition of NFκB signaling decreases RAGE expression in endothelial cells (44) and reduces Aβ production and BACE-1 expression levels (21,45,46).…”
Section: Discussionmentioning
confidence: 90%
“…The inhibition of NF-kB activation with an adenovirus-expressing IkBa mutation can attenuate HMGB1 translocation in cultured cells, as well as in a cecal ligation and puncture-induced animal model of sepsis (66). In addition, inhibitors of IKKa and IKKb have been shown to inhibit HMGB1-induced chemotaxis (67). In this study, the association between the increased levels of extracellular HMGB1 and hyperoxiainduced NF-kB activation suggests that NF-kB plays a role in oxidative stressinduced HMGB1 release.…”
Section: Ea Inhibits Hmgb1 Release From Hyperoxia-exposed Macrophagesmentioning
confidence: 99%