THE SMALL GTP-BINDING PROTEIN RAC REGULATES GROWTH-FACTOR INDUCED MEMBRANE RUFFLING
THE SMALL GTP-BINDING PROTEIN RAC REGULATES GROWTH-FACTOR INDUCED MEMBRANE RUFFLING
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DOI：
10.1016/0092-8674(92)90164-8
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发表时间：
1992-08-07
期刊：
影响因子：
64.5
通讯作者：
HALL, A
中科院分区：
文献类型：
--
作者：
RIDLEY, AJ;PATERSON, HF;HALL, A
用显微注射法研究了ras相关的GTP结合蛋白rac在成纤维细胞中的功能。在汇合血清饥饿瑞士3 T3细胞，rac 1迅速刺激肌动蛋白丝积累在质膜上，形成膜皱褶。几种生长因子和激活的H-ras也诱导膜皱褶，这种反应被阻止了显性抑制突变体外消旋蛋白，N17 rac 1。这表明内源性rac蛋白是生长因子诱导的膜皱褶所必需的。除了膜皱褶，后来的反应都rac 1显微注射和一些生长因子的肌动蛋白应力纤维的形成，需要内源性rho蛋白的过程。使用N17 rac 1，我们已经表明，这些生长因子的行为，通过外消旋刺激这种rho依赖性的反应。我们建议，外消旋体和rho的信号转导途径连接生长因子的组织聚合肌动蛋白的重要组成部分。
The function of rac, a ras-related GTP-binding protein, was investigated in fibroblasts by microinjection. In confluent serum-starved Swiss 3T3 cells, rac1 rapidly stimulated actin filament accumulation at the plasma membrane, forming membrane ruffles. Several growth factors and activated H-ras also induced membrane ruffling, and this response was prevented by a dominant inhibitory mutant rac protein, N17rac1. This suggests that endogenous rac proteins are required for growth factor-induced membrane ruffling. In addition to membrane ruffling, a later response to both rac1 microinjection and some growth factors was the formation of actin stress fibers, a process requiring endogenous rho proteins. Using N17rac1 we have shown that these growth factors act through rac to stimulate this rho-dependent response. We propose that rac and rho are essential components of signal transduction pathways linking growth factors to the organization of polymerized actin.