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首页> 外文期刊>Journal of Cellular Physiology >p38SJ, a novel DINGG protein protects neuronal cells from alcohol induced injury and death.
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p38SJ, a novel DINGG protein protects neuronal cells from alcohol induced injury and death.

机译:p38SJ,小说DINGG蛋白质保护神经元从酒精诱导细胞损伤和死亡。

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摘要

Ethanol induces neuronal cell injury and death by dysregulating several signaling events that are controlled, in part, by activation of MAPK/ERK1/2 and/or inactivation of its corresponding phosphatase, PP1. Recently, we have purified a novel protein of 38 kDa in size, p38SJ, from a callus culture of Hypericum perforatum, which belongs to an emerging DINGG family of proteins with phosphate binding activity. Here, we show that treatment of neuronal cells with p38SJ protects cells against injury induced by exposure to ethanol. Furthermore, pre-treatment of neuronal cells with p38SJ diminishes the level of the pro-apoptotic protein Bax and some events associated with apoptosis such as caspase 3 cleavage. In addition, by inducing stress, alcohol can elevate production of reactive oxygen species (ROS) that leads to a decrease in the activity of superoxide dismutase (SOD). Our results showed that p38SJ restores the activity of SOD in the ethanol treated neuronal cells. These observations provide a novel biological tool for developing new approaches for preventing neuronal cell death induced by ethanol and possibly treatment of neurological disorders associated with alcohol abuse.
机译:乙醇诱导神经细胞损伤和死亡就是说,几个信号事件控制,在一定程度上,通过激活MAPK / ERK1/2和/或其相应的失活磷酸酶,PP1。新颖的蛋白质大小38 kDa, p38SJ,从贯叶连翘的愈伤组织培养属于一个新兴DINGG家族的蛋白质与磷酸结合的活动。与p38SJ治疗神经细胞保护细胞免受损伤引起的风险乙醇。神经细胞与p38SJ减少的水平pro-apoptotic蛋白伯灵顿和一些事件半胱天冬酶3等与细胞凋亡有关分裂酒精可以提高活性氧的生产物种(ROS)导致下降超氧化物歧化酶(SOD)的活性。结果表明,p38SJ恢复活动乙醇处理SOD的神经元细胞。这些观察提供了一个新颖的生物为防止开发新方法的工具乙醇和引起的神经细胞死亡可能是治疗神经系统疾病与酗酒有关。

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