首页> 外文期刊>The European Journal of Neuroscience >Lack of alpha-synuclein does not alter apoptosis of neonatal catecholaminergic neurons.
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Lack of alpha-synuclein does not alter apoptosis of neonatal catecholaminergic neurons.

机译:缺乏α-突触核蛋白不会改变新生儿儿茶酚胺能神经元的凋亡。

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摘要

Abstract alpha-Synuclein is an abundant neuronal protein of uncertain function linked to Parkinson's disease. Numerous studies have proposed an antiapoptotic function for alpha-synuclein, based on overexpression experiments in cell lines. To explore whether alpha-synuclein has such a physiological function, we assessed the response of wild type or alpha-synuclein null neonatal mouse sympathetic neurons to nerve growth factor deprivation, a well-characterized stimulus of neuronal apoptosis. There was no difference in the rate of neuronal loss, neuronal apoptosis, or c-jun phosphorylation. Furthermore, the absence of alpha-synuclein did not alter the magnitude of naturally occurring cell death in vivo in substantia nigra pars compacta. Therefore, alpha-synuclein is unlikely to play a significant role in apoptotic signalling in catecholaminergic neurons of the neonatal nervous system.
机译:摘要α-突触核蛋白是与帕金森氏病有关的功能不确定的丰富神经元蛋白。基于细胞系中的过表达实验,许多研究提出了α-突触核蛋白的抗凋亡功能。为了探究α-突触核蛋白是否具有这种生理功能,我们评估了野生型或α-突触核蛋白无效的新生小鼠交感神经元对神经生长因子剥夺(神经元凋亡的一种充分表征的刺激)的反应。神经元丢失,神经元凋亡或c-jun磷酸化率没有差异。此外,不存在α-突触核蛋白不会改变黑质致密部体内体内自然发生的细胞死亡的程度。因此,α-突触核蛋白不太可能在新生儿神经系统的儿茶酚胺能神经元的凋亡信号传导中发挥重要作用。

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