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Nf1 RasGAP Inhibition of LIMK2 Mediates a New Cross-Talk between Ras and Rho Pathways

机译:LImK2介导的神经纤维瘤病rasGap的抑制的Ras和Rho途径之间一个新的交叉对话

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摘要

BackgroundRas GTPases mediate numerous biological processes through their ability to cycle between an inactive GDP-bound form and an active GTP-bound form. Guanine nucleotide exchange factors (GEFs) favor the formation of the active Ras-GTP, whereas GTPase activating proteins (GAPs) promote the formation of inactive Ras-GDP. Numerous studies have established complex signaling cross-talks between Ras GTPases and other members of the superfamily of small GTPases. GEFs were thought to play a major role in these cross-talks. However, recently GAPs were also shown to play crucial roles in these processes. Among RasGAPs, Nf1 is of special interest. Nf1 is responsible for the genetic disease Neurofibromatosis type I, and recent data strongly suggest that this RasGAP connects different signaling pathways.
机译:背景Ras GTPases通过其在非活性GDP结合形式和活性​​GTP结合形式之间循环的能力介导了许多生物过程。鸟嘌呤核苷酸交换因子(GEF)促进活性Ras-GTP的形成,而GTPase活化蛋白(GAPs)促进无活性Ras-GDP的形成。大量研究已经建立了Ras GTPases与小型GTPases超家族其他成员之间复杂的信号交互作用。人们认为,全球环境基金在这些相互影响中起主要作用。但是,最近还显示了GAP在这些过程中起着至关重要的作用。在RasGAP中,Nf1具有特别的意义。 Nf1导致遗传性疾病I型神经纤维瘤病,最近的数据强烈表明该RasGAP连接了不同的信号通路。

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