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http://purl.uniprot.org/citations/30958798http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30958798http://www.w3.org/2000/01/rdf-schema#comment"DCs undergo metabolic reprogramming from a predominantly oxidative phosphorylation (OXPHOS) to glycolysis to mount an immunogenic response. The mechanism underpinning the metabolic reprogramming remains elusive. We demonstrate that miRNA-142 (miR-142) is pivotal for this shift in metabolism, which regulates the tolerogenic and immunogenic responses of DCs. In the absence of miR-142, DCs fail to switch from OXPHOS and show reduced production of proinflammatory cytokines and the ability to activate T cells in vitro and in in vivo models of sepsis and alloimmunity. Mechanistic studies demonstrate that miR-142 regulates fatty acid (FA) oxidation, which causes the failure to switch to glycolysis. Loss- and gain-of-function experiments identified carnitine palmitoyltransferase -1a (CPT1a), a key regulator of the FA pathway, as a direct target of miR-142 that is pivotal for the metabolic switch. Thus, our findings show that miR-142 is central to the metabolic reprogramming that specifically favors glycolysis and immunogenic response by DCs."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.org/dc/terms/identifier"doi:10.1172/jci123839"xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Fujiwara H."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Kim S.H."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Sun Y."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Wu J."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Taylor A."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Bridges S."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Reddy P."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Saunders T."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Oravecz-Wilson K."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"McEachin R."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Peltier D.C."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/author"Zajac C."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/name"J Clin Invest"xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/pages"2029-2042"xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/title"miR-142 controls metabolic reprogramming that regulates dendritic cell activation."xsd:string
http://purl.uniprot.org/citations/30958798http://purl.uniprot.org/core/volume"129"xsd:string
http://purl.uniprot.org/citations/30958798http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30958798
http://purl.uniprot.org/citations/30958798http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30958798
http://purl.uniprot.org/uniprot/#_A0A1D8M9B3-mappedCitation-30958798http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30958798
http://purl.uniprot.org/uniprot/#_A0A0B6VTJ4-mappedCitation-30958798http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30958798
http://purl.uniprot.org/uniprot/#_A0A494B9G5-mappedCitation-30958798http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30958798