pubmed-article:12839997 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12839997 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
pubmed-article:12839997 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
pubmed-article:12839997 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:12839997 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:12839997 | pubmed:issue | 13 | lld:pubmed |
pubmed-article:12839997 | pubmed:dateCreated | 2003-7-3 | lld:pubmed |
pubmed-article:12839997 | pubmed:abstractText | It has been postulated that reactive oxygen species (ROS) may act as second messengers leading to nuclear factor (NF)-kappaB activation. This hypothesis is mainly based on the findings that N-acetyl-L-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), compounds recognized as potential antioxidants, can inhibit NF-kappaB activation in a wide variety of cell types. Here we reveal that both NAC and PDTC inhibit NF-kappaB activation independently of antioxidative function. NAC selectively blocks tumor necrosis factor (TNF)-induced signaling by lowering the affinity of receptor to TNF. PDTC inhibits the IkappaB-ubiquitin ligase activity in the cell-free system where extracellular stimuli-regulated ROS production does not occur. Furthermore, we present evidence that endogenous ROS produced through Rac/NADPH oxidase do not mediate NF-kappaB signaling, but instead lower the magnitude of its activation. | lld:pubmed |
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pubmed-article:12839997 | pubmed:language | eng | lld:pubmed |
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pubmed-article:12839997 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12839997 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12839997 | pubmed:month | Jul | lld:pubmed |
pubmed-article:12839997 | pubmed:issn | 0261-4189 | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:KarinMichaelM | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:TanakaHirofum... | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:MiyashitaHiro... | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:KikugawaKiyom... | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:KitagawaMasat... | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:YasudaHideyoH | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:HayakawaMakio... | lld:pubmed |
pubmed-article:12839997 | pubmed:author | pubmed-author:SakamotoIsaoI | lld:pubmed |
pubmed-article:12839997 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12839997 | pubmed:day | 1 | lld:pubmed |
pubmed-article:12839997 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:12839997 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12839997 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12839997 | pubmed:pagination | 3356-66 | lld:pubmed |
pubmed-article:12839997 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:12839997 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12839997 | pubmed:articleTitle | Evidence that reactive oxygen species do not mediate NF-kappaB activation. | lld:pubmed |
pubmed-article:12839997 | pubmed:affiliation | School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Tokyo 192-0392, Japan. | lld:pubmed |
pubmed-article:12839997 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12839997 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12839997 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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