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dc.contributor.author이영식-
dc.date.accessioned2018-02-28T00:02:20Z-
dc.date.available2018-02-28T00:02:20Z-
dc.date.issued2015-11-
dc.identifier.citationSCIENTIFIC REPORTS, v. 5, Article ID 16932en_US
dc.identifier.issn2045-2322-
dc.identifier.urihttps://www.nature.com/articles/srep16932-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/40919-
dc.description.abstractPersistent macrophage activation is associated with the expression of various pro-inflammatory genes, cytokines and chemokines, which may initiate or amplify inflammatory disorders. A novel synthetic BET inhibitor, JQ1, was proven to exert immunosuppressive activities in macrophages. However, a genome-wide search for JQ1 molecular targets has not been undertaken. The present study aimed at evaluating the anti-inflammatory function and underlying genes that are targeted by JQ1 in LPS-stimulated primary bone marrow-derived macrophages (BMDMs) using global transcriptomic RNA sequencing and quantitative real-time PCR. Among the annotated genes, transcriptional sequencing of BMDMs that were treated with JQ1 revealed a selective effect on LPS-induced gene expression in which the induction of cytokines/chemokines, interferon-stimulated genes, and prominent (transcription factors) TFs was suppressed. Additionally, we found that JQ1 reduced the expression of previously unidentified genes that are important in inflammation. Importantly, these inflammatory genes were not affected by JQ1 treatment alone. Furthermore, we confirmed that JQ1 reduced cytokines/chemokines in the supernatants of LPS treated BMDMs. Moreover, the biological pathways and gene ontology of the differentially expressed genes were determined in the JQ1 treatment of BMDMs. These unprecedented results suggest that the BET inhibitor JQ1 is a candidate for the prevention or therapeutic treatment of inflammatory disorders.en_US
dc.description.sponsorshipThis work was supported by a National Research Foundation of Korea (NRF) grant that was funded by the Korean government (MSIP) (2013R1A1A3011026 to K.H.J. & 2011-0030049 to Y.G.C.).en_US
dc.language.isoen_USen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectTUMOR-NECROSIS-FACTORen_US
dc.subjectDAP12-ASSOCIATING LECTIN (MDL)-1en_US
dc.subjectTOLL-LIKE RECEPTORSen_US
dc.subjectNF-KAPPA-Ben_US
dc.subjectRHEUMATOID-ARTHRITISen_US
dc.subjectSELECTIVE-INHIBITIONen_US
dc.subjectINNATE IMMUNITYen_US
dc.subjectFACTOR-ALPHAen_US
dc.subjectIRF FAMILYen_US
dc.subjectRNA-SEQen_US
dc.titleDual transcriptome sequencing reveals resistance of TLR4 ligand-activated bone marrow-derived macrophages to inflammation mediated by the BET inhibitor JQ1en_US
dc.typeArticleen_US
dc.relation.volume5-
dc.identifier.doi10.1038/srep16932-
dc.relation.page1-7-
dc.relation.journalSCIENTIFIC REPORTS-
dc.contributor.googleauthorDas, Amitabh-
dc.contributor.googleauthorChai, Jin Choul-
dc.contributor.googleauthorYang, Chul-su-
dc.contributor.googleauthorLee, Young Seek-
dc.contributor.googleauthorDas, Nando Dulal-
dc.contributor.googleauthorJung, Kyoung Hwa-
dc.contributor.googleauthorChai, Young Gyu-
dc.relation.code2015014066-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF SCIENCE AND CONVERGENCE TECHNOLOGY[E]-
dc.sector.departmentDEPARTMENT OF MOLECULAR AND LIFE SCIENCE-
dc.identifier.pidyslee-


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