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作 者:翁元峰 杨志彪[1] Weng Yuan-feng;Yang Zhi-biao(School of Agriculture and Biology,Shanghai Jiaotong University,Shanghai 200240;Institut Pasteur of Shanghai,Chinese Academy of Sciences,Shanghai 200031)
机构地区:[1]上海交通大学农业与生物学院,上海200240 [2]中国科学院上海巴斯德研究所,上海200031
出 处:《生物化工》2018年第5期147-149,共3页Biological Chemical Engineering
摘 要:Rap1是小GTPases蛋白中Ras家族中的成员之一,最开始是在全基因组检测中作为Ras转化过程中的抑制因子被发现的。在功能上,Rap1既可以干扰Ras蛋白介导的ERK活化,也可以不依赖于Ras蛋白而以细胞环境相关的方式激活ERK。越来越多的证据证明,Rap1是整合素的一种主要激活因子,在一系列依赖整合素的细胞功能中发挥调控作用。同时,如今也有重要的证据显示Rap1激活功能的调节异常是恶性肿瘤发展的重要原因。Rap1在很多种类型的细胞中会被不同的细胞外刺激因子所激活,但主要是受Rap1鸟嘌呤核苷酸交换因子(GEFs)和GTPase激活蛋白(GAPs)的调控。本文重点总结了Rap1在人类细胞中的生物学功能以及在其表达的调控因素。Rapl is a member of the Ras family of small GTPases, which was found originally in a genome-wide screen as suppressors of Ras transformation. Functionally, Rapl disturbs the Ras-mediated ERK activation, also activates ERK independently of Ras in a cell-circumstances dependent manner. Increasing evidence indicated that Rapl is a major activator of integrins, playing regulator roles in the regulation of a series of integrin-dependent cellular functions. Meanwhile, some significant evidence showed that dysregulation of Rapl activation is an important reason for the development of malignancy. Rap1 is activated by many extracellular stimuli, and regulated nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). In this review, we of studies of biological functions and regulation of Rapl in human cells.
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