Ral: Mediator of membrane trafficking
Ral: Mediator of membrane trafficking
复制标题
DOI：
10.1016/j.biocel.2006.04.006
复制
发表时间：
2006-01-01
影响因子：
4
通讯作者：
Robinson, Phillip J.
中科院分区：
文献类型：
--
作者：
van Dam, Ellen M.;Robinson, Phillip J.
Ral是一种多功能的小GT酶，参与肿瘤发生和控制细胞内膜运输。它主要由Ras下游的因子激活，或独立于这些因子，并通过与扩展的伴侣库的蛋白质-蛋白质相互作用来运作。RalA是通过结合磷脂酶D的钙诱发的胞吐的正调节剂，并且通过结合磷脂酶C-δ 1参与G蛋白偶联受体信号传导。Ral与钙调蛋白的结合与细胞内运输事件有关。另一个联系是活化的Ral（Ral-GTP）与内吞和外吞机制的直接结合。Ral-GTP结合RalBP 1，RalBP 1通过AP-2连接到受体介导的内吞作用。或者，Ral-GTP结合外囊复合物，其控制调节分泌和丝状伪足形成中的分泌囊泡运输。因此，Ral-GTP在不同的膜运输途径之间“选择”。Ral的其他合作伙伴仍在探索中，这可能会为Ral如何控制不同的膜运输途径提供进一步的机制见解。(c)2006爱思唯尔有限公司保留所有权利。
Ral is a multifunctional small GTPase involved in tumorigenesis and in controlling intracellular membrane trafficking. It is mainly activated by factors downstream of Ras, or independently of these factors and operates by protein-protein interactions with an expanding repertoire of partners. RalA is a positive regulator of calcium-evoked exocytosis via binding phospholipase D and is involved in G protein coupled receptor signalling by binding phospholipase C-delta 1. The binding of Ral to calmodulin links to intracellular trafficking events. Another link is direct binding of activated Ral (Ral-GTP) to the endocytic and exocytic machineries. Ral-GTP binds RalBP1, which connects to receptor-mediated endocytosis via AP-2. Alternatively, Ral-GTP binds the exocyst complex, which controls secretory vesicle trafficking in regulated secretion and filopodia formation. Thus, Ral-GTP "chooses" between different membrane trafficking pathways. Other Ral partners are still being uncovered that may provide further mechanistic insights into how Ral controls diverse membrane trafficking pathways. (c) 2006 Elsevier Ltd. All rights reserved.