ArfGAP family proteins in cell adhesion, migration and tumor invasion
ArfGAP family proteins in cell adhesion, migration and tumor invasion
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DOI：
10.1016/j.ceb.2006.08.002
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发表时间：
2006-10-01
影响因子：
7.5
通讯作者：
Hashimoto, Shigeru
中科院分区：
文献类型：
--
作者：
Sabe, Hisataka;Onodera, Yasuhito;Hashimoto, Shigeru
几种 ArfGAP 蛋白被鉴定为桩蛋白（一种整联蛋白信号传导和支架蛋白）的结合伴侣，这表明整联蛋白功能和细胞内运输之间存在分子联系，正如 MS Bretscher 很久以前提出的那样。在结合桩蛋白的 ArfGAP 中，AMAP1 最近与肿瘤侵袭和恶性肿瘤密切相关，因为它在肿瘤中表达高度增强，并且直接参与侵袭活动。另一个 ArfGAP，Git2，被发现是 G beta gamma 介导的定向传感机制的一个组成部分，同时在抑制控制超氧化物产生中发挥着重要作用，超氧化物产生是由 GPCR 刺激的中性粒细胞中的囊泡运输介导的。这些新兴的分子机制可能进一步描述调节细胞内交通的关键过程作为细胞运动和侵袭活动的主要控制。
The identification of several ArfGAP proteins as binding partners of paxillin, an integrin signaling and scaffolding protein, has suggested the existence of molecular links between integrin functions and intracellular traffic, as proposed by MS Bretscher long ago. Among the paxillin-binding ArfGAPs, AMAP1 has recently been strongly implicated in tumor invasion as well as malignancy, owing to its highly augmented expression in tumors and its direct involvement in invasive activities. Another ArfGAP, Git2, was found to be a component of the G beta gamma-mediated directional sensing machinery, while simultaneously playing an essential role in the suppressive control of superoxide production, which is mediated by vesicle transport in GPCR-stimulated neutrophils. These emerging molecular mechanisms may further delineate key processes regulating intracellular traffic as principal controls of cell motility and invasive activities.