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别构自激活 SOS 及其动力学机制。

Allosteric autoactivation of SOS and its kinetic mechanism.

机构信息

Department of Chemistry and Biochemistry, The University of Texas at Arlington , Arlington, TX, USA.

出版信息

Small GTPases. 2021 Jan;12(1):44-59. doi: 10.1080/21541248.2019.1601954. Epub 2019 Apr 13.

Abstract

Son of Sevenless (SOS), one of guanine nucleotide exchange factors (GEFs), activates Ras. We discovered that the allosteric domain of SOS yields SOS to proceed a previously unrecognized autoactivation kinetics. Its essential feature is a time-dependent acceleration of SOS feedback activation with a reaction initiator or with the priming of active Ras. Thus, this mechanistic autoactivation feature explains the notion, previously only conjectured, of accelerative SOS activation followed by the priming of active Ras, an action produced by another GEF Ras guanyl nucleotide-releasing protein (RasGRP). Intriguingly, the kinetic transition from gradual RasGRP activation to accelerative SOS activation has been interpreted as an analog to digital conversion; however, from the perspective of autoactivation kinetics, it is a process of straightforward RasGRP-mediated SOS autoactivation. From the viewpoint of allosteric protein cooperativity, SOS autoactivation is a unique time-dependent cooperative SOS activation because it enables an active SOS to accelerate activation of other SOS as a function of time. This time-dependent SOS cooperativity does not belong to the classic steady-state protein cooperativity, which depends on ligand concentration. Although its hysteretic or sigmoid-like saturation curvature is a classic hallmark of steady-state protein cooperativity, its hyperbolic saturation figure typically represents protein noncooperativity. We also discovered that SOS autoactivation perturbs the previously predicted hysteresis of SOS activation in a steady state to produce a hyperbolic saturation curve. We interpret this as showing that SOS allostery elicits, through SOS autoactivation, cooperativity uniquely time-dependent but not ligand concentration dependent.

摘要

SOS,一种鸟嘌呤核苷酸交换因子(GEFs)的儿子,激活 Ras。我们发现 SOS 的变构域使 SOS 进行以前未被识别的自动激活动力学。其基本特征是 SOS 反馈激活的时间依赖性加速,具有反应引发剂或活性 Ras 的引发作用。因此,这种机械自动激活特性解释了以前仅推测的加速 SOS 激活,随后是活性 Ras 的引发作用,这是另一种 GEF Ras 鸟嘌呤核苷酸释放蛋白(RasGRP)产生的作用。有趣的是,从逐渐的 RasGRP 激活到加速的 SOS 激活的动力学转变已被解释为模拟到数字的转换;然而,从自动激活动力学的角度来看,这是一个直接的 RasGRP 介导的 SOS 自动激活过程。从变构蛋白协同作用的角度来看,SOS 自动激活是一种独特的时间依赖性协同 SOS 激活,因为它使活性 SOS 能够加速其他 SOS 的激活,这是时间的函数。这种时间依赖性的 SOS 协同作用不属于依赖配体浓度的经典稳态蛋白协同作用。尽管其滞后或类似 S 形的饱和曲率是经典稳态蛋白协同作用的标志,但它的双曲线饱和图通常代表蛋白质非协同作用。我们还发现 SOS 自动激活会干扰稳态下以前预测的 SOS 激活滞后,从而产生双曲线饱和曲线。我们将其解释为表明 SOS 变构通过 SOS 自动激活引发独特的时间依赖性协同作用,但不依赖配体浓度。

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Kinetic Mechanism of Formation of Hyperactive Embryonic Ras in Cells.细胞中高活性胚胎型Ras形成的动力学机制。
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