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一种轴突切断诱导的糖基化蛋白AIGP1的鉴定,其可能参与内质网-高尔基体应激引发的细胞死亡。

Identification of an axotomy-induced glycosylated protein, AIGP1, possibly involved in cell death triggered by endoplasmic reticulum-Golgi stress.

作者信息

Aoki Shunsuke, Su Qingning, Li Hang, Nishikawa Kaori, Ayukawa Kohichi, Hara Yoko, Namikawa Kazuhiko, Kiryu-Seo Sumiko, Kiyama Hiroshi, Wada Keiji

机构信息

Department of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-8502, Japan.

出版信息

J Neurosci. 2002 Dec 15;22(24):10751-60. doi: 10.1523/JNEUROSCI.22-24-10751.2002.

Abstract

We developed a new method, designated N-linked glycosylation signal (NGS) differential display (DD)-PCR, that enables the identification of genes encoding N-linked glycosylated molecules that exhibit varying patterns of expression. Using this innovative technique, we identified an N-linked glycosylated 11-transmembrane domain protein that is upregulated in response to axotomy. Expression levels increased 3 d after axotomy, reached maximal levels at approximately postoperative days 5-7, and then gradually decreased through day 20. The protein was termed axotomy-induced glycosylated/Golgi-complex protein 1 (AIGP1). AIGP1 immunoreactivity is specifically localized in neurons, with subcellular localization within the Golgi, indicating that AIGP1 is a resident Golgi protein. Moreover, AIGP1 gene expression in cultured neurons is specifically induced by the endoplasmic reticulum (ER)-Golgi stressors tunicamycin and brefeldin A. We observed that the frequency of cell death is increased by AIGP1 overexpression and that the corresponding region of the protein implicated in the activity involves the large eighth and ninth transmembrane loops. Our results suggest that AIGP1 gene activation and protein accumulation in the Golgi complex in response to axotomy-induced ER-Golgi stress may contribute to signaling during programmed cell death in damaged neurons.

摘要

我们开发了一种新方法,命名为N-连接糖基化信号(NGS)差异显示(DD)-PCR,该方法能够鉴定编码具有不同表达模式的N-连接糖基化分子的基因。利用这项创新技术,我们鉴定出一种N-连接糖基化的11跨膜结构域蛋白,其在轴突切断后上调。轴突切断后3天表达水平升高,在术后约5-7天达到最高水平,然后在第20天逐渐下降。该蛋白被命名为轴突切断诱导糖基化/高尔基体复合蛋白1(AIGP1)。AIGP1免疫反应性特异性定位于神经元中,亚细胞定位在高尔基体中,表明AIGP1是一种驻留高尔基体蛋白。此外,内质网(ER)-高尔基体应激剂衣霉素和布雷菲德菌素A可特异性诱导培养神经元中AIGP1基因表达。我们观察到AIGP1过表达会增加细胞死亡频率,并且该蛋白中与活性相关的相应区域涉及第八和第九个大跨膜环。我们的结果表明,轴突切断诱导的ER-高尔基体应激导致AIGP1基因激活和蛋白在高尔基体复合物中积累,这可能在受损神经元程序性细胞死亡过程中发挥信号传导作用。

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