Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이지희 | * |
dc.date.accessioned | 2018-05-18T08:14:52Z | - |
dc.date.available | 2018-05-18T08:14:52Z | - |
dc.date.issued | 2005 | * |
dc.identifier.issn | 1528-7394 | * |
dc.identifier.other | OAK-2891 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/243050 | - |
dc.description.abstract | Involvement of protein tyrosine kinases (PTK) in lipopolysaccharide (LPS)-induced nuclear factor-kappa B (NF- B) activation has been demonstrated. Studies investigated the role of PTK and the underlying mechanisms by which PTK play a role in LPS induction of pathways leading to NF- B activation in macrophages. Inhibitors of PTK - genistein, herbimycin A, or AG126 - blocked LPS-induced NF- B activation. Genistein also blocked pervanadate-induced NF- B activation. Furthennore, Src TK selective inhibitors - damnacanthal or PP1 - blocked LPS-induced NF- B activation over a range of nanomolar concentrations. Genistein, damnacanthal, or PP1 blocked the LPS-induced serine phosphorylation, the degradation of I B- , and the consequent translocation of the p65 subunit of NF- B to the nucleus. In addition to serine phosphorylation of I B- , LPS-induced NF- B activation also required tyrosine phosphorylation of I B- . These TK inhibitors blocked substantially LPS induction of tyrosine phosphorylation of I B- . Furthermore, cSrc and Lck were physically associated with I B- . These results suggest that the LPS-induced NF- B pathways are dependent on both serine and tyrosine phosphorylation of I B- , and that Src TK, such as cSrc and Lck, are key components of the LPS signaling pathway through at least two different mechanisms associated with NF- B activation. Copyright© Taylor & Francis Inc. | * |
dc.language | English | * |
dc.title | Inhibition of Src tyrosine kinases suppresses activation of nuclear factor-κB, and serine and tyrosine phosphorylation of IκB-α in lipopolysaccharide-stimulated raw 264.7 macrophages | * |
dc.type | Article | * |
dc.relation.issue | 19 | * |
dc.relation.volume | 68 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1643 | * |
dc.relation.lastpage | 1662 | * |
dc.relation.journaltitle | Journal of Toxicology and Environmental Health - Part A | * |
dc.identifier.doi | 10.1080/15287390500192114 | * |
dc.identifier.wosid | WOS:000231614400004 | * |
dc.identifier.scopusid | 2-s2.0-26944445087 | * |
dc.author.google | Kang J.L. | * |
dc.author.google | Hye W.L. | * |
dc.author.google | Hee J.K. | * |
dc.author.google | Hui S.L. | * |
dc.author.google | Castranova V. | * |
dc.author.google | Lim C.-M. | * |
dc.author.google | Koh Y. | * |
dc.contributor.scopusid | 이지희(7404517577) | * |
dc.date.modifydate | 20240116125728 | * |