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http://purl.uniprot.org/citations/15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15020650http://www.w3.org/2000/01/rdf-schema#comment"Monocyte chemoattractant protein-1 (MCP-1, CCL2) is a mediator of inflammation that has been implicated in the pathogenesis of a wide variety of human diseases. CCR2, a heterotrimeric G-coupled receptor, is the only known receptor that functions at physiologic concentrations of MCP-1. Despite the importance of CCR2 in mediating MCP-1 responses, several recent studies have suggested that there may be another functional MCP-1 receptor. Using arterial smooth muscle cells (SMC) from CCR2(-/-) mice, we demonstrate that MCP-1 induces tissue-factor activity at physiologic concentrations. The induction of tissue factor by MCP-1 is blocked by pertussis toxin and 1,2-bis(O-aminophenyl-ethane-ethan)-N,N,N',N'-tetraacetic acid-acetoxymethyl ester, suggesting that signal transduction through the alternative receptor is G(alphai)-coupled and dependent on mobilization of intracellular Ca(2+). MCP-1 induces a time- and concentration-dependent phosphorylation of the mitogen-activated protein kinases p42/44. The induction of tissue factor activity by MCP-1 is blocked by PD98059, an inhibitor of p42/44 activation, but not by SB203580, a selective p38 inhibitor. These data establish that SMC possess an alternative MCP-1 receptor that signals at concentrations of MCP-1 that are similar to those that activate CCR2. This alternative receptor may be important in mediating some of the effects of MCP-1 in atherosclerotic arteries and in other inflammatory processes."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.org/dc/terms/identifier"doi:10.1189/jlb.0903421"xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Ma H."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Yi L."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Schecter A.D."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Charo I.F."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Soejima K."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Rollins B.J."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Taubman M.B."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Daly C.M."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/author"Berman A.B."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/name"J Leukoc Biol"xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/pages"1079-1085"xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/title"MCP-1-dependent signaling in CCR2(-/-) aortic smooth muscle cells."xsd:string
http://purl.uniprot.org/citations/15020650http://purl.uniprot.org/core/volume"75"xsd:string
http://purl.uniprot.org/citations/15020650http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15020650
http://purl.uniprot.org/citations/15020650http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15020650
http://purl.uniprot.org/uniprot/#_P63085-mappedCitation-15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15020650
http://purl.uniprot.org/uniprot/#_A0A338P736-mappedCitation-15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15020650
http://purl.uniprot.org/uniprot/#_A0A338P781-mappedCitation-15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15020650
http://purl.uniprot.org/uniprot/#_A0A0U1RPX4-mappedCitation-15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15020650
http://purl.uniprot.org/uniprot/#_A0A0U1RPZ0-mappedCitation-15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15020650
http://purl.uniprot.org/uniprot/#_D3Z3G6-mappedCitation-15020650http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15020650