| http://purl.uniprot.org/citations/29860267 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29860267 | http://www.w3.org/2000/01/rdf-schema#comment | "Multiple sclerosis and its primary animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory diseases of the central nervous system (CNS) characterized by immune-mediated demyelination and neurodegeneration that may be mediated by inhibition of the nuclear factor-κB (NF-κB) signaling pathway. Gpr97, encoded by Adgrg3, has been reported to regulate the activity of NF-κB. In this study, using a previously established Adgrg3-knockout mouse model, we investigated the roles of Gpr97 in the development of autoimmune CNS disease in mice. We found a marked increase in the expression of Adgrg3 in spinal cords of mice with EAE. Adgrg3-deficient (Adgrg3-/-) mice with EAE exhibited increases in peak severity and the cumulative disease score compared with littermate controls, followed by a notable increase of leukocyte infiltration and more extensive demyelination. The percentages of Th1/Th17 cells in the CNS were significantly increased in Adgrg3-/-mice and accompanied by high levels of interleukin (IL)-6, interferon-γ, tumor necrosis factor-α, and IL-17. An in vitro culture assay verified that Gpr97 regulated proinflammatory cytokine production. Taken together, our results show that Gpr97 plays an important role in the development of EAE and may have a therapeutic potential for the treatment of CNS autoimmunity."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.org/dc/terms/identifier | "doi:10.1093/abbs/gmy060"xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Chen X."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Lu S."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Wang J."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Wang Z."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Kuang Y."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/author | "Fei J."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/name | "Acta Biochim Biophys Sin (Shanghai)"xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/pages | "666-675"xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/title | "Gpr97/Adgrg3 ameliorates experimental autoimmune encephalomyelitis by regulating cytokine expression."xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://purl.uniprot.org/core/volume | "50"xsd:string |
| http://purl.uniprot.org/citations/29860267 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29860267 |
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