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http://purl.uniprot.org/citations/25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25908843http://www.w3.org/2000/01/rdf-schema#comment"Macrophages mediate innate immune responses that recognise foreign pathogens, and bacterial lipopolysaccharide (LPS) recruits a signalling pathway through Toll-like receptor 4 (TLR4) to induce pro-inflammatory cytokines and reactive oxygen species (ROS). LPS activation also skews the metabolism of macrophages towards a glycolytic phenotype. Here, we demonstrate that the LPS-triggered glycolytic switch is significantly attenuated in macrophages deficient for glutathione transferase omega-1 (GSTO1, note that GSTO1-1 refers to the dimeric molecule with identical type 1 subunits). In response to LPS, GSTO1-1-deficient macrophages do not produce excess lactate, or dephosphorylate AMPK, a key metabolic stress regulator. In addition, GSTO1-1-deficient cells do not induce HIF1α, which plays a key role in maintaining the pro-inflammatory state of activated macrophages. The accumulation of the TCA cycle intermediates succinate and fumarate that occurs in LPS-treated macrophages was also blocked in GSTO1-1-deficient cells. These data indicate that GSTO1-1 is required for LPS-mediated signalling in macrophages and that it acts early in the LPS-TLR4 pro-inflammatory pathway."xsd:string
http://purl.uniprot.org/citations/25908843http://purl.org/dc/terms/identifier"doi:10.1242/jcs.167858"xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/author"O'Neill L.A."xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/author"Board P.G."xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/author"Menon D."xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/author"Coll R."xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/name"J Cell Sci"xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/pages"1982-1990"xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/title"GSTO1-1 modulates metabolism in macrophages activated through the LPS and TLR4 pathway."xsd:string
http://purl.uniprot.org/citations/25908843http://purl.uniprot.org/core/volume"128"xsd:string
http://purl.uniprot.org/citations/25908843http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25908843
http://purl.uniprot.org/citations/25908843http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25908843
http://purl.uniprot.org/uniprot/#_A2BHU8-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_L0CL36-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_O09131-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_L0CMZ8-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_Q3U4D4-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_Q8K2T5-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_U5LHT3-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_V9PC02-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_V9PC04-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_V9PC06-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843
http://purl.uniprot.org/uniprot/#_Q9QUK6-mappedCitation-25908843http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25908843