| http://purl.uniprot.org/citations/24486434 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24486434 | http://www.w3.org/2000/01/rdf-schema#comment | "Non-receptor protein tyrosine kinases (NRPTKs)-dependent inflammatory signal transduction cascades play key roles in immunoregulation. However, drug intervention through NRPTKs-involved immunoregulation mechanism in microglia (the major immune cells of the central nervous system) has not been widely investigated. A main aim of the present study is to elucidate the contribution of two major NRPTKs (Syk and Jak2) in neuroinflammation suppression by a bioactive sesquiterpene dimmer (DSF-27). We found that LPS-stimulated BV-2 cells activated Syk and further initiated Akt/NF-κB inflammatory pathway. This Syk-dependent Akt/NF-κB inflammatory pathway can be effectively ameliorated by DSF-27. Moreover, Jak2 was activated by LPS, which was followed by transcriptional factor Stat3 activation. The Jak2/Stat3 signal was suppressed by DSF-27 through inhibition of Jak2 and Stat3 phosphorylation, promotion of Jak/Stat3 inhibitory factors PIAS3 expression, and down-regulation of ERK and p38 MAPK phosphorylation. Furthermore, DSF-27 protected cortical and mesencephalic dopaminergic neurons against neuroinflammatory injury. Taken together, our findings indicate NRPTK signaling pathways including Syk/NF-κB and Jak2/Stat3 cascades are potential anti-neuroinflammatory targets in microglia, and may also set the basis for the use of sesquiterpene dimmer as a therapeutic approach for neuroinflammation via interruption of these pathways."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.taap.2014.01.014"xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/author | "Dong X."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/author | "Jiang Y."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/author | "Wang S."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/author | "Jin H.W."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/author | "Tu P.F."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/author | "Zeng K.W."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/name | "Toxicol Appl Pharmacol"xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/pages | "244-256"xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/title | "Sesquiterpene dimmer (DSF-27) inhibits the release of neuroinflammatory mediators from microglia by targeting spleen tyrosine kinase (Syk) and Janus kinase 2 (Jak2): Two major non-receptor tyrosine signaling proteins involved in inflammatory events."xsd:string |
| http://purl.uniprot.org/citations/24486434 | http://purl.uniprot.org/core/volume | "275"xsd:string |
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