The mechanistic link between Arc/Arg3.1 expression and AMPA receptor endocytosis.
The mechanistic link between Arc/Arg3.1 expression and AMPA receptor endocytosis.
复制标题
DOI：
10.1016/j.semcdb.2017.09.005
复制
发表时间：
2017-09
影响因子：
7.3
通讯作者：
Mark J. Wall;Sonia A. L. Corrêa
中科院分区：
文献类型：
--
作者：
Mark J. Wall;Sonia A. L. Corrêa
活性调节细胞骨架相关蛋白 (Arc/Arg3.1) 通过促进 AMPA 受体 (AMPAR) 内吞作用在决定突触强度方面发挥着关键作用。尽管关于电弧感应控制突触可塑性和学习行为的机制有大量数据，但仍然存在一些关键的机制问题。在这里，我们回顾了 Arc 表达与网格蛋白介导的内吞 AMPAR 途径之间联系的数据，并讨论了 Arc 与网格蛋白接头蛋白 2 (AP-2) 和内亲蛋白/动力蛋白结合的重要性。我们考虑哪些 AMPAR 亚基被选择用于 Arc 介导的内化、对突触功能的影响，并将 Arc 视为治疗靶点。
The activity-regulated cytoskeleton associated protein (Arc/Arg3.1) plays a key role in determining synaptic strength through facilitation of AMPA receptor (AMPAR) endocytosis. Although there is considerable data on the mechanism by which Arc induction controls synaptic plasticity and learning behaviours, several key mechanistic questions remain. Here we review data on the link between Arc expression and the clathrin-mediated endocytic pathway which internalises AMPARs and discuss the significance of Arc binding to the clathrin adaptor protein 2 (AP-2) and to endophilin/dynamin. We consider which AMPAR subunits are selected for Arc-mediated internalisation, implications for synaptic function and consider Arc as a therapeutic target.