Control of Rho GTPase function by BAR-domains.

Control of Rho GTPase function by BAR-domains.
复制标题

DOI:
10.4161/sgtp.18960
复制
发表时间:
2012-01
期刊:
影响因子:
--
通讯作者:
Hordijk PL
Hordijk PL
中科院分区:
其他
文献类型:
--
作者:
de Kreuk BJ;Hordijk PL

文献摘要

被引文献

相似文献

细胞骨架动力学是建立细胞极性和随后协调驱动细胞迁移的突出和收缩的关键。在这些事件中,肌动蛋白和微管细胞骨架与控制胞内和胞吐作用的细胞机制协同作用,从而调节膜和膜相关蛋白的极化运输。Rho家族的小GTP酶协调细胞骨架动力学。Rho GT3信号传导受到严格调控,并且错误定位或组成性激活可能导致例如形态发生异常、肿瘤细胞转移或凋亡。越来越多的证据表明,进出质膜的交通构成了控制Rho GT3激活和信号传导的重要机制。这个简要的概述讨论了一组蛋白质,在膜动力学和RhoGTdR信号之间的接口功能。这些蛋白质都共享一个所谓的BAR结构域,这是一个脂质和蛋白质结合区域,也具有膜变形活性。在过去的15年中,越来越多的BAR结构域蛋白被鉴定并发现调节Rho GT3信号传导。这里讨论的研究定义了几种模式的RhoGTdR调控通过BAR域含有蛋白质,识别BAR域作为一个重要的调节单元桥接膜交通和细胞骨架动力学。
Cytoskeletal dynamics are key to the establishment of cell polarity and the consequent coordination of protrusion and contraction that drives cell migration. During these events, the actin and microtubule cytoskeleton act in concert with the cellular machinery that controls endo-and exocytosis, thus regulating polarized traffic of membranes and membrane-associated proteins. Small GTPases of the Rho family orchestrate cytoskeletal dynamics. Rho GTPase signaling is tightly regulated and mislocalization or constitutive activation may lead to, for example, morphogenetic abnormalities, tumor cell metastasis or apoptosis. There is increasing evidence that traffic to and from the plasma membrane constitutes an important mechanism controlling Rho GTPase activation and signaling. This brief overview discusses a group of proteins that function at the interface between membrane dynamics and RhoGTPase signaling. These proteins all share a so-called BAR domain, which is a lipid and protein binding region that also harbors membrane deforming activity. In the past 15 years, a growing number of BAR domain proteins have been identified and found to regulate Rho GTPase signaling. The studies discussed here define several modes of RhoGTPase regulation through BAR-domain containing proteins, identifying the BAR domain as an important regulatory unit bridging membrane traffic and cytoskeletal dynamics.