| http://purl.uniprot.org/citations/17012367 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17012367 | http://www.w3.org/2000/01/rdf-schema#comment | "The procoagulant thrombin promotes polymorphonuclear leukocyte (PMN) adhesion to endothelial cells by a mechanism involving expression of intercellular adhesion molecule-1 (ICAM-1) via an NF-kappaB-dependent pathway. We now provide evidence that activation of c-Src is crucial in signaling thrombin-induced ICAM-1 expression via tyrosine phosphorylation of RelA/p65. Stimulation of human umbilical vein endothelial cells with thrombin resulted in a time-dependent activation of c-Src, with maximal activation occurring at 30 min after thrombin challenge. Inhibition of c-Src by pharmacological and genetic approaches impaired thrombin-induced NF-kappaB-dependent reporter activity and ICAM-1 expression. Analysis of the NF-kappaB pathway revealed that the effect of c-Src inhibition occurred independently of IkappaBalpha degradation and NF-kappaB DNA binding function and was not associated with exchange of NF-kappaB dimers. Phosphorylation of RelA/p65 at Ser(536), an event mediating the transcriptional activity of DNA-bound RelA/p65, was also insensitive to c-Src inhibition. Interestingly, thrombin induced association of c-Src with RelA/p65, and inhibition of c-Src prevented this response, indicating that this interaction is contingent on activation of c-Src. We also observed that thrombin induced tyrosine phosphorylation of RelA/p65, and this phosphorylation was lost upon inhibition of c-Src, consistent with the requirement of activated c-Src for interaction with RelA/p65. These data implicate an important role of c-Src in phosphorylating RelA/p65 to promote the transcriptional activity of NF-kappaB and thereby ICAM-1 expression in endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajplung.00163.2006"xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/author | "Rahman A."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/author | "Fazal F."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/author | "O'Reilly M.A."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/author | "Platanias L.C."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/author | "Bijli K.M."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/author | "Minhajuddin M."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/name | "Am J Physiol Lung Cell Mol Physiol"xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/pages | "L396-404"xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/title | "c-Src interacts with and phosphorylates RelA/p65 to promote thrombin-induced ICAM-1 expression in endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://purl.uniprot.org/core/volume | "292"xsd:string |
| http://purl.uniprot.org/citations/17012367 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17012367 |
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