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首页> 外文期刊>IBRO Reports >Abnormal activation of NMDA receptors by Glufosinate ammonium
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Abnormal activation of NMDA receptors by Glufosinate ammonium

机译:草铵膦铵盐对NMDA受体的异常激活

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However, the underlying mechanism about JEV triggers neuronal cell apopto- sis remains unclear. The objective of this study was to investigate the JEV infection of human neuroblastoma SH-SY5Y cells including virus replication and virus-induced neuronal cell death. The result demonstrated that the virus replicated in time-dependent pattern and the progressive of JEV replication was related to the induction of cell death which obviously presented at the late period of infec- tion. Interestingly, the expression levels of the p18 Bax, the cleaved form of Bax, was markedly increased whereas the full-length Bax expression was gradually decreased which corresponded to the increase of neuronal cell death during JEV infection. The formation of truncated p18 Bax appeared to be associated with JEV-triggered neuronal cell death. This novel finding provides another possible mechanism of JEV-induced apoptosis which could lead to further therapeutic developments for alleviating the neuronal injury from the infection of JEV.
机译:但是,关于JEV触发神经元细胞凋亡的潜在机制仍不清楚。这项研究的目的是调查人类神经母细胞瘤SH-SY5Y细胞的JEV感染,包括病毒复制和病毒诱导的神经元细胞死亡。结果表明,病毒以时间依赖性方式复制,JEV复制的进行与细胞死亡的诱导有关,这显然是在感染后期出现的。有趣的是,p18 Bax(Bax的裂解形式)的表达水平显着增加,而全长Bax表达则逐渐降低,这与JEV感染期间神经元细胞死亡的增加相对应。截短的p18 Bax的形成似乎与JEV触发的神经元细胞死亡有关。该新发现提供了JEV诱导的细胞凋亡的另一种可能的机制,其可能导致减轻JEV感染引起的神经元损伤的进一步治疗发展。

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