http://purl.uniprot.org/citations/21187453 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/21187453 | http://www.w3.org/2000/01/rdf-schema#comment | "Ligand activation of liver X receptors (LXRs) has been shown to impact both lipid metabolism and inflammation. One complicating factor in studies utilizing synthetic LXR agonists is the potential for pharmacologic and receptor-independent effects. Here, we describe an LXR gain-of-function system that does not depend on the addition of exogenous ligand. We generated transgenic mice expressing a constitutively active VP16-LXRα protein from the aP2 promoter. These mice exhibit increased LXR signaling selectively in adipose and macrophages. Analysis of gene expression in primary macrophages derived from two independent VP16-LXRα transgenic lines confirmed the ability of LXR to drive expression of genes involved in cholesterol efflux and fatty acid synthesis. Moreover, VP16-LXRα expression also suppressed the induction of inflammatory genes by lipopolysaccharide to a comparable degree as synthetic agonist. We further utilized VP16-LXRα-expressing macrophages to identify and validate new targets for LXRs, including the gene encoding ADP-ribosylation factor-like 7 (ARL7). ARL7 has previously been shown to transport cholesterol to the membrane for ABCA1-associated removal and thus may be integral to the LXR-dependent efflux pathway. We show that the ARL7 promoter contains a functional LXRE and can be transactivated by LXRs in a sequence-specific manner, indicating that ARL7 is a direct target of LXR. These findings provide further support for an important role of LXRs in the coordinated regulation of lipid metabolic and inflammatory gene programs in macrophages."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.org/dc/terms/identifier | "doi:10.1194/jlr.m010686"xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Hong C."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Tontonoz P."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Bradley M.N."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Walczak R."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Boyadjian R."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Marathe C."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Dhamko H."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/author | "Salazar J.V."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/name | "J Lipid Res"xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/pages | "531-539"xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/title | "Constitutive activation of LXR in macrophages regulates metabolic and inflammatory gene expression: identification of ARL7 as a direct target."xsd:string |
http://purl.uniprot.org/citations/21187453 | http://purl.uniprot.org/core/volume | "52"xsd:string |
http://purl.uniprot.org/citations/21187453 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/21187453 |
http://purl.uniprot.org/citations/21187453 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/21187453 |
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http://purl.uniprot.org/uniprot/#_A0A140LIH8-mappedCitation-21187453 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/21187453 |