| http://purl.uniprot.org/citations/15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15265939 | http://www.w3.org/2000/01/rdf-schema#comment | "Proinflammatory cytokine (e.g., TNF-alpha)-induced expression of endothelial cell adhesion molecules (ECAMs) on the lumenal surface of the vascular endothelium and a consequent increase in leukocyte adhesion are key aspects of pathological inflammation. A promising therapeutic approach to diminish aberrant leukocyte adhesion is, therefore, to inhibit cytokine-induced ECAM expression at the transcription level. Several studies suggest that methimazole, a compound used clinically to treat autoimmune diseases, such as Graves' disease, may also diminish pathological inflammation by suppressing ECAM expression. In this study we probed the hypothesis that a derivative of methimazole, phenyl methimazole (compound 10), can reduce cytokine-induced ECAM expression and consequent leukocyte adhesion. We found that compound 10 1) dramatically inhibits TNF-alpha-induced VCAM-1 mRNA and protein expression in human aortic endothelial cells (HAEC), has a relatively modest inhibitory effect on TNF-alpha induced E-selectin expression and has no effect on ICAM-1 expression; 2) significantly reduces TNF-alpha-induced monocytic (U937) cell adhesion to HAEC under in vitro flow conditions similar to that present in vivo; 3) inhibits TNF-alpha-induced IFN regulatory factor-1 binding to VCAM-1 promoter; and 4) reduces TNF-alpha-induced IRF-1 expression in HAEC. Combined, the results indicate that phenyl methimazole can reduce TNF-alpha-induced VCAM-1 expression in an IFN regulatory factor-1-dependent manner and that this contributes significantly to reduced monocytic cell adhesion to TNF-alpha-activated HAEC."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.173.3.2041"xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Sun X."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Kohn L.D."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Lewis C.J."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Harii N."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Goetz D.J."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Dagia N.M."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/author | "Meli A.E."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/pages | "2041-2049"xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/title | "Phenyl methimazole inhibits TNF-alpha-induced VCAM-1 expression in an IFN regulatory factor-1-dependent manner and reduces monocytic cell adhesion to endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://purl.uniprot.org/core/volume | "173"xsd:string |
| http://purl.uniprot.org/citations/15265939 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15265939 |
| http://purl.uniprot.org/citations/15265939 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15265939 |
| http://purl.uniprot.org/uniprot/#_A0A0B6XK53-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_A0A0B6XK11-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_A0A1B1RS94-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_A0A510GDD8-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_B4DQF0-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_P10914-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_Q59F37-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |
| http://purl.uniprot.org/uniprot/#_Q75MZ8-mappedCitation-15265939 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15265939 |