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Roles of protrudin at interorganelle membrane contact sites.
Proceedings of the Japan Academy, Series B ( IF 4.4 ) Pub Date : 2019-01-01 , DOI: 10.2183/pjab.95.023
Michiko Shirane 1
Affiliation  

Intracellular organelles were long viewed as isolated compartments floating in the cytosol. However, this view has been radically changed within the last decade by the discovery that most organelles communicate with the endoplasmic reticulum (ER) network via membrane contact sites (MCSs) that are essential for intracellular homeostasis. Protrudin is an ER resident protein that was originally shown to regulate neurite formation by promoting endosome trafficking. More recently, however, protrudin has been found to serve as a tethering factor at MCSs. The roles performed by protrudin at MCSs are mediated by its various domains, including inactivation of the small GTPase Rab11, bending of the ER membrane, and functional interactions with other molecules such as the motor protein KIF5 and the ER protein VAP. Mutations in the protrudin gene (ZFYVE27) are associated with hereditary spastic paraplegia, an axonopathy that results from defective ER structure. This review, examines the pleiotropic molecular functions of protrudin and its role in interorganellar communication.

中文翻译:

胃泌素在器官间膜接触部位的作用。

长期以来,人们一直将细胞内细胞器视为漂浮在细胞质溶胶中的孤立隔室。但是,由于发现大多数细胞器通过细胞内稳态必不可少的膜接触位点(MCS)与内质网(ER)网络通信,这种观点在过去十年中已发生了根本性的改变。Protrudin是一种ER驻留蛋白,最初被证明可通过促进内体运输来调节神经突的形成。然而,最近,在MCS上发现抑菌素是束缚因子。protrudin在MCSs上发挥的作用由其各种域介导,包括小GTPase Rab11的失活,ER膜的弯曲以及与其他分子(例如运动蛋白KIF5和ER蛋白VAP)的功能性相互作用。蛋白原蛋白基因(ZFYVE27)的突变与遗传性痉挛性截瘫有关,这是一种由ER结构缺陷导致的轴索病。这项审查,审查了protrudin的多效性分子功能及其在组织间通讯中的作用。
更新日期:2019-11-01
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