Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이지희 | * |
dc.contributor.author | 김형래 | * |
dc.contributor.author | 이경은 | * |
dc.date.accessioned | 2018-05-30T08:14:06Z | - |
dc.date.available | 2018-05-30T08:14:06Z | - |
dc.date.issued | 2006 | * |
dc.identifier.issn | 1096-6080 | * |
dc.identifier.other | OAK-3223 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243512 | - |
dc.description.abstract | Protein tyrosine kinases (PTKs) and mitogen-activated protein kinases (MAPKs) have been demonstrated to play a crucial role in the signaling pathways induced by silica. In the present study, we investigated whether Src family TKs play a role in crystalline silica-induced NF-κB activation and whether NF-κB activation requires Src TK-dependent MAPK activity in RAW 264.7 cells, a mouse peritoneal macrophage cell line. Selective Src TK inhibitors, damnacanthal or PP1, inhibited silica-induced NF-κB activation in a dose-dependent manner. Furthermore, these kinase inhibitors suppressed silica-induced tyrosine phosphorylation of IκB-α and p65 NF-κB. Within a similar time frame, c-Src and Lck were physically associated with IκB-α and with p65 NF-κB. Silica stimulated the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2), but not p38 MAPK and c-Jun NH2-terminal kinase 1 and 2 (JNK1/2). Damnacanthal or PP1 substantially blocked the silica-induced activation of ERK1/2. Moreover, PD98059, an inhibitor of ERK1/2, or SB203580, an inhibitor of p38 MAPK, failed to inhibit silica-induced NF-κB activation. These results suggest that c-Src and Lck act for silica-induced NF-κB activation by mediating the tyrosine phosphorylations of IκB-α and p65 NF-κB. However, the Src TK-dependent activation of ERK1/2 may not be involved in the silica signaling pathway leading to NF-κB activation. © 2006 Oxford University Press. | * |
dc.language | English | * |
dc.title | Src tyrosine kinases mediate crystalline silica-induced NF-κB activation through tyrosine phosphorylation of IκB-α and p65 NF-κB in rAW 264.7 macrophages | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 90 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 470 | * |
dc.relation.lastpage | 477 | * |
dc.relation.journaltitle | Toxicological Sciences | * |
dc.identifier.doi | 10.1093/toxsci/kfj096 | * |
dc.identifier.wosid | WOS:000236106000021 | * |
dc.identifier.scopusid | 2-s2.0-33645129200 | * |
dc.author.google | Kang J.L. | * |
dc.author.google | Jung H.J. | * |
dc.author.google | Lee K. | * |
dc.author.google | Kim H.R. | * |
dc.contributor.scopusid | 이지희(7404517577) | * |
dc.contributor.scopusid | 김형래(57202558385;57219111690;57567109600) | * |
dc.contributor.scopusid | 이경은(7409769243) | * |
dc.date.modifydate | 20240118123830 | * |