| http://purl.uniprot.org/citations/11776328 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11776328 | http://www.w3.org/2000/01/rdf-schema#comment | "Plasminogen activator inhibitor-1 (PAI-1) is a serine protease inhibitor (SERPIN) specific for tissue-type and urokinase-like plasminogen activators. High plasma PAI-1 activity is a risk factor for thrombotic diseases. Due to the short half-life of PAI-1, regulation of PAI-1 gene expression and secretion of active PAI-1 into the blood stream is important for hemostatic balance. We have investigated transcriptional control of PAI-1 gene expression in bovine aortic endothelial cells (BAECs) and human cell lines using PAI-1 5' promoter-luciferase reporter assays. Contrary to the cytokine-induced up-regulation of PAI-1 mRNA and protein levels, we found that only transforming growth factor-beta (TGF-beta) was efficient in inducing PAI-1 promoter activation. Tissue necrosis factor-alpha (TNF-alpha) induced a small luciferase activity with the 2.5 kb PAI-1 promoter, but not with the PAI-800/4G/5G and p3TP-lux promoters. Next we investigated whether a lack of response to TNF-alpha was due to deficient signaling pathways. BAECs responded to TNF-alpha with robust NFkappaB promoter activation. TGF-beta activated the p38 MAP kinase, while TNF-alpha activated both the SAPK/JNK and p38 MAP kinases. The ERK1/2 MAP kinases were constitutively activated in BAECs. BAEC therefore responded to TNF-alpha stimulation with activation of the MAP kinases and the NFkappaB transcriptional factors. We further measured the messenger RNA stability under the influence by TGF-beta and TNF-alpha and found no difference. PAI-1 gene activation by TNF-alpha apparently is yet to be defined for the location of the response element and/or the signaling pathway, while TGF-beta is the most important cytokine for PAI-1 transcriptional activation through its 5' proximal promoter."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/author | "Chen Y.Q."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/author | "Tseng-Crank J."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/author | "Richardson M.A."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/author | "Sloan-Lancaster J."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/author | "Grinnell B."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/author | "Berg D.T."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/name | "Thromb Haemost"xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/pages | "1563-1572"xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/title | "Differential mechanisms of plasminogen activator inhibitor-1 gene activation by transforming growth factor-beta and tumor necrosis factor-alpha in endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://purl.uniprot.org/core/volume | "86"xsd:string |
| http://purl.uniprot.org/citations/11776328 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11776328 |
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