| http://purl.uniprot.org/citations/24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24462864 | http://www.w3.org/2000/01/rdf-schema#comment | "Microglia are immune cells that maintain brain homeostasis at a resting state by surveying the environment and engulfing debris. However, in some pathological conditions, microglia can produce neurotoxic factors such as pro-inflammatory cytokines and nitric oxide (NO) that lead to neuronal degeneration. Inflammation-induced calcium (Ca(2+)) signaling is thought to underlie this abnormal activation of microglia, but the mechanisms are still obscure. We previously showed that combined application of lipopolysaccharide and interferon γ (LPS/IFNγ) induced-production of NO in microglia from wild-type (WT) mice is significantly reduced in microglia from transient receptor potential melastatin 2 (TRPM2)-knockout (KO) mice. Here, we found that LPS/IFNγ produced a late-onset Ca(2+) signaling in WT microglia, which was abolished by application of the NADPH oxidase inhibitor diphenylene iodonium (DPI) and ML-171. In addition, pharmacological blockade or gene deletion of TRPM2 channel in microglia did not show this Ca(2+) signaling. Furthermore, pharmacological manipulation and Western blotting revealed that Ca(2+) mobilization, the proline-rich tyrosine kinase 2 (Pyk2), p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun NH2-terminal kinase (JNK) contributed to TRPM2-mediated LPS/IFNγ-induced activation, while the extracellular signal-regulated protein kinase (ERK) did not. These results suggest that LPS/IFNγ activates TRPM2-mediated Ca(2+) signaling, which in turn increases downstream p38 MAPK and JNK signaling and results in increased NO production in microglia."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2014.01.022"xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Mori Y."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Nakagawa T."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Kaneko S."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Miyake T."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Konno M."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Kusano A."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Shirakawa H."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/author | "Sakimoto S."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/pages | "212-217"xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/title | "TRPM2 contributes to LPS/IFNgamma-induced production of nitric oxide via the p38/JNK pathway in microglia."xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://purl.uniprot.org/core/volume | "444"xsd:string |
| http://purl.uniprot.org/citations/24462864 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24462864 |
| http://purl.uniprot.org/citations/24462864 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24462864 |
| http://purl.uniprot.org/uniprot/#_D3Z7Q7-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |
| http://purl.uniprot.org/uniprot/#_D3Z1Z4-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |
| http://purl.uniprot.org/uniprot/#_A0A3B2WAZ7-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |
| http://purl.uniprot.org/uniprot/#_A0A3B2WB60-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |
| http://purl.uniprot.org/uniprot/#_A0A1W2P6F5-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |
| http://purl.uniprot.org/uniprot/#_A0A2I3BPL3-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |
| http://purl.uniprot.org/uniprot/#_A3KBF5-mappedCitation-24462864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24462864 |