Ras-ERK 和 PI3K-mTOR 通路：串扰和补偿。
The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation.
机构信息
Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
出版信息
Trends Biochem Sci. 2011 Jun;36(6):320-8. doi: 10.1016/j.tibs.2011.03.006. Epub 2011 Apr 30.
Abstract
The Ras-extracellular signal-regulated kinase (Ras-ERK) and phosphatidylinositol 3-kinase-mammalian target of rapamycin (PI3K-mTOR) signaling pathways are the chief mechanisms for controlling cell survival, differentiation, proliferation, metabolism, and motility in response to extracellular cues. Components of these pathways were among the first to be discovered when scientists began cloning proto-oncogenes and purifying cellular kinase activities in the 1980s. Ras-ERK and PI3K-mTOR were originally modeled as linear signaling conduits activated by different stimuli, yet even early experiments hinted that they might intersect to regulate each other and co-regulate downstream functions. The extent of this cross-talk and its significance in cancer therapeutics are now becoming clear.
摘要
Ras-细胞外信号调节激酶（Ras-ERK）和磷脂酰肌醇 3-激酶-雷帕霉素靶蛋白（PI3K-mTOR）信号通路是控制细胞存活、分化、增殖、代谢和运动的主要机制，以响应细胞外信号。这些通路的组成部分是科学家在 20 世纪 80 年代开始克隆原癌基因和纯化细胞激酶活性时首先发现的。Ras-ERK 和 PI3K-mTOR 最初被建模为不同刺激激活的线性信号传导途径，但即使是早期实验也暗示它们可能交叉调节彼此，并共同调节下游功能。这种串扰的程度及其在癌症治疗学中的意义现在变得越来越清楚。
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