Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/70812
標題: Japanese encephalitis virus infection stimulates Src tyrosine kinase in neuron/glia
作者: Raung, S.L.
Chen, S.Y.
Liao, S.L.
Chen, J.H.
Chen, C.J.
關鍵字: Japanese encephalitis virus
inflammation
protein tyrosine kinase
Src
kinase
tumor-necrosis-factor
astrocyte-enriched cultures
nf-kappa-b
gene-expression
family kinases
signaling pathway
nitric-oxide
mixed
glia
t-cells
protein
期刊/報告no:: Neuroscience Letters, Volume 419, Issue 3, Page(s) 263-268.
摘要: Japanese 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.
URI: http://hdl.handle.net/11455/70812
ISSN: 0304-3940
文章連結: http://dx.doi.org/10.1016/j.neulet.2007.04.036
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