On the molecular basis for mechanotransduction.

R. Kamm, M. Kaazempur-Mofrad
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引用次数: 63

Abstract

Much is currently known about the signaling pathways that are excited when cells are subjected to a mechanical stimulus, yet we understand little of the process by which the mechanical perturbation is transformed into a biochemical signal. Numerous theories have been proposed, and each has merit. While cells may possess many different ways of responding to stress, the existence of a single unifying principle has much appeal. Here we propose the hypothesis that cells sense mechanical force through changes in protein conformation, leading to altered binding affinities of proteins, ultimately initiating an intracellular signaling cascade or producing changes in the proteins localized to regions of high stress. More generally, this represents an alternative to transmembrane signaling through receptor-ligand interactions providing the cell with a means of reacting to changes in its mechanical, as opposed to biochemical, environment. One example is presented showing how the binding affinity between the focal adhesion targeting domain of focal adhesion kinase and the LD motif of paxillin is influenced by externally applied force.
论机械传导的分子基础。
当细胞受到机械刺激时,信号通路被激发,目前我们知道的很多,但我们对机械扰动转化为生化信号的过程知之甚少。人们提出了许多理论,每种理论都有其优点。虽然细胞可能有许多不同的方式来应对压力,但存在一个统一的原则是很有吸引力的。在这里,我们提出了一种假设,即细胞通过改变蛋白质的构象来感知机械力,从而改变蛋白质的结合亲和力,最终启动细胞内信号级联或产生位于高应激区域的蛋白质的变化。更一般地说,这代表了一种通过受体-配体相互作用的跨膜信号的替代方法,为细胞提供了一种对其机械环境(而不是生化环境)变化作出反应的手段。一个例子显示了焦点粘附激酶的焦点粘附靶向区域与paxillin的LD基序之间的结合亲和力如何受到外力的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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