Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/70812
DC FieldValueLanguage
dc.contributor.authorRaung, S.L.en_US
dc.contributor.authorChen, S.Y.en_US
dc.contributor.authorLiao, S.L.en_US
dc.contributor.authorChen, J.H.en_US
dc.contributor.authorChen, C.J.en_US
dc.date2007zh_TW
dc.date.accessioned2014-06-11T06:00:24Z-
dc.date.available2014-06-11T06:00:24Z-
dc.identifier.issn0304-3940zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/70812-
dc.description.abstractJapanese encephalitis virus (JEV) is a neurotropic virus. The clinically manifestation of JEV-induced encephalitis is characterized by the brain inflammation and neuronal dysfunction and/or destruction. Currently, the cellular signaling molecules that underlie JEV-induced cerebral inflammation and cellular alterations are not well understood. Protein tyrosine phosphorylation events are key regulators of cellular signaling processes, including inflammation. We investigated whether Src protein tyrosine kinase (PTK) function in JEV-induced cellular chances in neuron/glia cultures. JEV infection modulated tyrosine phosphorylation events. Src PTK was hyperphosphorylated at the early stage of infection. Biochemical studies demonstrated that both inhibitors of the Src family PTK and Ras attenuated JEV-induced extracellular signal-regulated kinase (ERK) activation. Our results further revealed that PTK, Ras, and ERK inhibitors effectively suppressed JEV-induced pro-inflammatory cytokine expression and neurotoxicity. Pharmacological studies suggested that microglia secreted pro-inflammatory cytokine via Src/Ras/ERK pathway in responding to JEV infection. Another interesting observation was that nonstructural protein 3 (NS3) was able to interact with Src and showed tyrosine phosphorylation. However, the biological consequences of their interaction and exact control of NS3 tyrosine phosphorylation required further investigation. Our results suggest that the Src/Ras/ERK signaling cascade is involved in JEV-induced pro-inflammatory cytokine expression and neurotoxicity. (C) 2007 Elsevier Ireland Ltd. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationNeuroscience Lettersen_US
dc.relation.ispartofseriesNeuroscience Letters, Volume 419, Issue 3, Page(s) 263-268.en_US
dc.relation.urihttp://dx.doi.org/10.1016/j.neulet.2007.04.036en_US
dc.subjectJapanese encephalitis virusen_US
dc.subjectinflammationen_US
dc.subjectprotein tyrosine kinaseen_US
dc.subjectSrcen_US
dc.subjectkinaseen_US
dc.subjecttumor-necrosis-factoren_US
dc.subjectastrocyte-enriched culturesen_US
dc.subjectnf-kappa-ben_US
dc.subjectgene-expressionen_US
dc.subjectfamily kinasesen_US
dc.subjectsignaling pathwayen_US
dc.subjectnitric-oxideen_US
dc.subjectmixeden_US
dc.subjectgliaen_US
dc.subjectt-cellsen_US
dc.subjectproteinen_US
dc.titleJapanese encephalitis virus infection stimulates Src tyrosine kinase in neuron/gliaen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.neulet.2007.04.036zh_TW
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en_US-
item.fulltextno fulltext-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
Appears in Collections:期刊論文
Show simple item record
 

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.