| http://purl.uniprot.org/citations/28574596 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28574596 | http://www.w3.org/2000/01/rdf-schema#comment | "GPR84, a member of the G protein-coupled receptor family, is found predominantly in immune cells, such as macrophages, and functions as a pivotal modulator of inflammatory responses. In this study, we investigated the role of GPR84 in receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation. Our microarray data showed that GPR84 was significantly downregulated in osteoclasts compared to in their precursors, macrophages. The overexpression of GPR84 in bone marrow-derived macrophages suppressed the formation of multinucleated osteoclasts without affecting precursor proliferation. In addition, GPR84 overexpression attenuated the induction of c-Fos and nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), which are transcription factors that are critical for osteoclastogenesis. Furthermore, knockdown of GPR84 using a small hairpin RNA promoted RANKL-mediated osteoclast differentiation and gene expression of osteoclastogenic markers. Mechanistically, GPR84 overexpression blocked RANKL-stimulated phosphorylation of IκBα and three MAPKs, JNK, ERK, and p38. GPR84 also suppressed NF-κB transcriptional activity mediated by RANKL. Conversely, GPR84 knockdown enhanced RANKL-induced activation of IκBα and the three MAPKs. Collectively, our results revealed that GPR84 functions as a negative regulator of osteoclastogenesis, suggesting that it may be a potential therapeutic target for osteoclast-mediated bone-destructive diseases."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.26035"xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Kim H.J."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Lee H.W."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Yoon H.J."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Cho S."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Park J.W."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Kang W.Y."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Seong S.J."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/author | "Yoon Y.R."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/pages | "1481-1489"xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/title | "G protein-coupled receptor 84 controls osteoclastogenesis through inhibition of NF-kappaB and MAPK signaling pathways."xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://purl.uniprot.org/core/volume | "233"xsd:string |
| http://purl.uniprot.org/citations/28574596 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28574596 |
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