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http://purl.uniprot.org/citations/21268089http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21268089http://www.w3.org/2000/01/rdf-schema#comment"PPARs and LXRs are ligand-activated transcription factors that are emerging as promising therapeutic targets for limiting atherosclerosis, an inflammatory disorder orchestrated by cytokines. The potent anti-atherogenic actions of these nuclear receptors involve the regulation of glucose and lipid metabolism along with attenuation of the inflammatory response. Similarly, cholesterol-lowering drugs, statins, inhibit inflammation. Unfortunately, the mechanisms underlying such inhibitory actions of these agents in human macrophages are poorly understood and were therefore investigated in relation to IFN-γ, a key pro-atherogenic cytokine, which mediates its cellular effects mainly through STAT1. Simvastatin and PPAR agonists had no effect on the IFN-γ-induced, phosphorylation-mediated activation of STAT1 and its DNA binding but attenuated its ability to activate gene transcription. On the other hand, LXR activators attenuated both DNA binding and trans-activation potential of STAT1 induced by IFN-γ. These studies reveal differences in the mechanism of action of agonists of PPARs (and simvastatin) and LXRs on the IFN-γ-induced, STAT1-mediated gene transcription in human macrophages."xsd:string
http://purl.uniprot.org/citations/21268089http://purl.org/dc/terms/identifier"doi:10.1002/jcb.22976"xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/author"Li N."xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/author"Ramji D.P."xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/author"Salter R.C."xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/name"J Cell Biochem"xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/pages"675-683"xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/title"Molecular mechanisms underlying the inhibition of IFN-gamma-induced, STAT1-mediated gene transcription in human macrophages by simvastatin and agonists of PPARs and LXRs."xsd:string
http://purl.uniprot.org/citations/21268089http://purl.uniprot.org/core/volume"112"xsd:string
http://purl.uniprot.org/citations/21268089http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21268089
http://purl.uniprot.org/citations/21268089http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21268089
http://purl.uniprot.org/uniprot/P55055#attribution-F1FC6BDD3B65F62AC8D32B2499F7DE61http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21268089
http://purl.uniprot.org/uniprot/Q13133#attribution-F1FC6BDD3B65F62AC8D32B2499F7DE61http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21268089
http://purl.uniprot.org/uniprot/P37231#attribution-E52BC8290F7518A4FB9FA1C2378D0CA5http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21268089
http://purl.uniprot.org/uniprot/P42224#attribution-4079CA398175FCCFA5F5584E1BF0B947http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/21268089