pubmed-article:16177180 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C2348867 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:16177180 | lifeskim:mentions | umls-concept:C2728259 | lld:lifeskim |
pubmed-article:16177180 | pubmed:issue | 16 | lld:pubmed |
pubmed-article:16177180 | pubmed:dateCreated | 2005-9-22 | lld:pubmed |
pubmed-article:16177180 | pubmed:abstractText | Activation of the transcription factor NF-kappaB is critical for the tumor necrosis factor-alpha (TNF-alpha)-induced inflammatory response. Here we report the complete gene expression profile from activated microvascular endothelial cells emphasizing the direct contribution of the NF-kappaB pathway. Human microvascular endothelial cell line-1 (HMEC-1) cells were modified to express dominant interfering mutants of the IKK/NF-kappaB signaling module and expression profiles were determined. Our results provide compelling evidence for the virtually absolute dependence of TNF-alpha-regulated genes on NF-kappaB. A constitutively active IKK2 was sufficient for maximal induction of most target genes, whereas a transdominant IkappaBalpha suppressed gene expression. Several genes with a critical role in atherogenesis were identified. The endothelial lipase (EL) gene, a key enzyme involved in lipoprotein metabolism, was investigated more in detail. Binding sites interacting with NF-kappaB in vitro and in vivo were identified and co-transfection experiments demonstrated the direct regulation of the EL promoter by NF-kappaB. We conclude that targeting the IKK/NF-kappaB pathway or specific genes downstream may be effective for the control or prevention of chronic inflammatory diseases such as atherosclerosis. | lld:pubmed |
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pubmed-article:16177180 | pubmed:language | eng | lld:pubmed |
pubmed-article:16177180 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16177180 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16177180 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16177180 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16177180 | pubmed:issn | 1362-4962 | lld:pubmed |
pubmed-article:16177180 | pubmed:author | pubmed-author:WirthThomasT | lld:pubmed |
pubmed-article:16177180 | pubmed:author | pubmed-author:KempeSybilleS | lld:pubmed |
pubmed-article:16177180 | pubmed:author | pubmed-author:KestlerHansH | lld:pubmed |
pubmed-article:16177180 | pubmed:author | pubmed-author:LasarAndreaA | lld:pubmed |
pubmed-article:16177180 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:16177180 | pubmed:volume | 33 | lld:pubmed |
pubmed-article:16177180 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16177180 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16177180 | pubmed:pagination | 5308-19 | lld:pubmed |
pubmed-article:16177180 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:16177180 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:16177180 | pubmed:articleTitle | NF-kappaB controls the global pro-inflammatory response in endothelial cells: evidence for the regulation of a pro-atherogenic program. | lld:pubmed |