The US3 protein kinase of herpes simplex virus attenuates the activation of the c-Jun N-terminal protein kinase signal transduction pathway in infected piriform cortex neurons of C57BL/6 mice
The US3 protein kinase of herpes simplex virus attenuates the activation of the c-Jun N-terminal protein kinase signal transduction pathway in infected piriform cortex neurons of C57BL/6 mice
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DOI：
10.1016/j.neulet.2003.08.033
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发表时间：
2003-11
影响因子：
2.5
通讯作者：
I. Mori;F. Goshima;T. Koshizuka;N. Koide;T. Sugiyama;T. Yoshida;T. Yokochi;Y. Kimura;Y. Nishiyama
中科院分区：
文献类型：
--
作者：
I. Mori;F. Goshima;T. Koshizuka;N. Koide;T. Sugiyama;T. Yoshida;T. Yokochi;Y. Kimura;Y. Nishiyama
将单纯疱疹病毒（HSV）立体定向显微注射到小鼠嗅球中，导致梨状皮质神经元感染。野生型HSV感染的神经元没有明显的c-Jun N-末端蛋白激酶（JNK）/c-Jun磷酸化，而L1 BR 1病毒US 3基因破坏的突变体感染的神经元则以核染色的方式显示JNK/c-Jun磷酸化。与L1 BR 1病毒相比，野生型HSV诱导神经细胞凋亡被部分抑制。US 3拯救的L1 B −11病毒分离株表现与野生型病毒相同。总的来说，单纯疱疹病毒的US 3蛋白激酶在减弱病毒诱导的中枢神经系统JNK信号转导途径的激活方面发挥作用，并且可能至少部分有助于控制神经元细胞凋亡。
Stereotaxic microinjection of herpes simplex virus (HSV) into the mouse olfactory bulb resulted in infection of neurons of the piriform cortex. Neurons infected with the wildtype HSV showed no evident phosphorylation of c-Jun N-terminal protein kinase (JNK)/c-Jun. In contrast, neurons infected with a US3 gene-disrupted mutant of the L1BR1 virus displayed phosphorylated JNK/c-Jun in a nuclear staining fashion. Induction of neuronal apoptosis by the wildtype HSV was partially suppressed when compared with that of the L1BR1 virus. A US3-rescued isolate of the L1B−11 virus behaved as did the wildtype virus. Collectively, the US3 protein kinase of HSV plays a role in attenuating the virus-induced activation of the JNK signal transduction pathway in the central nervous system and may contribute, at least in part, to controlling neuronal apoptosis.