Trafficking cascades mediated by Rab35 and its membrane hub effector, MICAL-L1.
Trafficking cascades mediated by Rab35 and its membrane hub effector, MICAL-L1.
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DOI：
10.4161/cib.20064
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发表时间：
2012-07-01
影响因子：
--
通讯作者：
Caplan S
中科院分区：
文献类型：
--
作者：
Giridharan SS;Cai B;Naslavsky N;Caplan S
不同的受体在进入质膜的过程中穿过内吞循环室(ERC)。它们通过从ERC发出的表现出不同管状形态的循环内小体运输。该领域的一个关键问题是如何调控通过这些内体进行的贩运，以及Rab35、Rab8、Arf6和EHD1等调节蛋白如何控制这种贩运。最近的研究表明，Mical-L1蛋白是这些调控因子的主要支架。Mical-L1不仅定位于这些肾小管循环内小体并调节转运，而且还控制EHD1和Rab8对这些结构的定位。它还通过其结合伙伴CRMP2将其相关的膜连接到马达蛋白动力蛋白和动力蛋白。我们最近的研究促进了Mical-L1作为Rab35效应器的作用，其中Rab35通过Arf6直接或间接地控制Mical-L1和Rab8在肾小管膜上的定位。我们发现Mical-L1是一个多任务的支架，将各种蛋白质连接到循环内小体，以进行有效的运输。
Various receptors navigate through the endocytic recycling compartment (ERC) on route to the plasma membrane. They are transported through recycling endosomes that emanate from the ERC that display distinct tubular morphology. A key question in the field is how the trafficking via these endosomes is regulated and how regulatory proteins such as Rab35, Rab8, Arf6 and EHD1 control this trafficking. Recent studies point to the protein MICAL-L1 as a major scaffold for these regulators. MICAL-L1 not only localizes to these tubular recycling endosomes and regulates trafficking, but it also controls the localization of EHD1 and Rab8 to these structures. It also connects its associated membranes to the motor proteins dynein and kinesin through its binding partner, CRMP2. Our recent study promotes MICAL-L1 as a Rab35 effector, where Rab35, both directly and indirectly through Arf6, controls the localization of MICAL-L1 and Rab8 to tubular membranes. We find that MICAL-L1 is a multi-tasking scaffold connecting various proteins to recycling endosomes for efficient trafficking.