Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이지희 | * |
dc.date.accessioned | 2016-08-28T11:08:33Z | - |
dc.date.available | 2016-08-28T11:08:33Z | - |
dc.date.issued | 2000 | * |
dc.identifier.issn | 0041-008X | * |
dc.identifier.other | OAK-578 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218723 | - |
dc.description.abstract | It was previously reported that protein tyrosine kinase (PTK) but not protein kinase C or A plays an important role in silica-induced activation of NF-κB in macrophages. The question is raised whether PTK stimulation and NF-κB activation in silica-stimulated macrophages are directly connected through tyrosine phosphorylation of IκB-α. Results indicate that stimulation of macrophages with silica led to NF-κB activation through tyrosine phosphorylation without serine phosphorylation. Specific inhibitors of protein tyrosine kinase, such as genistein and tyrophostin AG126, prevented tyrosine phosphorylation of IκB-α in response to silica. IκB-α protein levels remained relatively unchanged for up to 60 min after silica stimulation. Moreover, inhibition of proteasome proteolytic activity did not affect NF-κB activation by silica. Antioxidants, such as superoxide dismutase (SOD), N-acetylcysteine (NAC), and pyrrolidine dithiocarbamate (PDTC), blocked tyrosine phosphorylation of IκB-α induced by silica, suggesting reactive oxygen species (ROS) may be important regulatory molecules in NF-κB activation through tyrosine phosphorylation of IκB-α. The results suggest that tyrosine phosphorylation of IκB-α represents a proteasome proteolytic activity-independent mechanism for NF-κB activation that directly couples NF-κB to cellular tyrosine kinase in silica-stimulated macrophages. This proposed mechanism of NF-κB activation induced by silica could be used as a target for development of antiinflammatory and antifibrosis drugs. (C) 2000 Academic Press. | * |
dc.language | English | * |
dc.title | Silica induces nuclear factor-κB activation through tyrosine phosphorylation of IκB-α in RAW264.7 macrophages | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 169 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 59 | * |
dc.relation.lastpage | 65 | * |
dc.relation.journaltitle | Toxicology and Applied Pharmacology | * |
dc.identifier.doi | 10.1006/taap.2000.9039 | * |
dc.identifier.wosid | WOS:000165627600008 | * |
dc.identifier.scopusid | 2-s2.0-0034669120 | * |
dc.author.google | Kang J.L. | * |
dc.author.google | Pack I.S. | * |
dc.author.google | Hong S.M. | * |
dc.author.google | Lee H.S. | * |
dc.author.google | Castranova V. | * |
dc.contributor.scopusid | 이지희(7404517577) | * |
dc.date.modifydate | 20240116125728 | * |