The ubiquitin-proteasome system regulates the stability of neuronal nicotinic acetylcholine receptors.
The ubiquitin-proteasome system regulates the stability of neuronal nicotinic acetylcholine receptors.
复制标题
DOI：
10.1007/s12031-009-9272-x
复制
发表时间：
2010-01
期刊：
影响因子：
--
通讯作者：
De Biasi M
中科院分区：
文献类型：
--
作者：
Rezvani K;Teng Y;De Biasi M
泛素化是蛋白酶体系统降解蛋白质、膜蛋白内化和细胞间蛋白质运输的关键事件。关于泛素-蛋白酶体系统（UPS）在神经元烟碱乙酰胆碱受体（nAChRs）运输中的作用的数据很少。在神经元样分化大鼠嗜铬细胞瘤细胞（PC12细胞）中进行的实验表明，α3、β2和β4 nAChR亚基被泛素化，并且它们的泛素化是降解所必需的。用蛋白酶体抑制剂PS-341处理24小时后，全细胞裂解物和内质网/高尔基区富集的部分中α3和两个β亚基的总水平均升高。在质膜富集组分中也检测到nAChR亚基上调。E-64对溶酶体降解机制的抑制作用对nAChR周转率的影响较小。目前的数据，加上之前的结果表明α7 nAChR亚基是UPS的靶标，表明蛋白酶体在nAChR转运中起着突出作用。
Ubiquitination is a key event for protein degradation by the proteasome system, membrane protein internalization, and protein trafficking among cellular compartments. Few data are available on the role of the ubiquitin–proteasome system (UPS) in the trafficking of neuronal nicotinic acetylcholine receptors (nAChRs). Experiments conducted in neuron-like differentiated rat pheochromocytoma cells (PC12 cells) show that the α3, β2, and β4 nAChR subunits are ubiquitinated and that their ubiquitination is necessary for degradation. A 24-h treatment with the proteasome inhibitor PS-341 increased the total levels of α3 and the two β subunits in both whole cell lysates and fractions enriched for the ER/Golgi compartment. nAChR subunit upregulation was also detected in plasma membrane-enriched fractions. Inhibition of the lysosomal degradation machinery by E-64 had a significantly smaller effect on nAChR turnover. The present data, together with previous results showing that the α7 nAChR subunit is a target of the UPS, point to a prominent role of the proteasome in nAChR trafficking.
登录
查看更多内容
影响因子：
3.5
作者：
Fujita, Eriko;Kouroku, Yoriko;Momoi, Takashi
通讯作者：
Momoi, Takashi
影响因子：
11.4
作者：
Eimer, Stefan;Gottschalk, Alexander;Bessereau, Jean-Louis
通讯作者：
Bessereau, Jean-Louis
影响因子：
7.8
作者：
Beck, T;Schmidt, A;Hall, MN
通讯作者：
Hall, MN
影响因子：
4.7
作者：
Castelan, Francisco;Castillo, Mar;Criado, Manuel
通讯作者：
Criado, Manuel
影响因子：
16.2
作者：
Ehlers, MD
通讯作者：
Ehlers, MD