Molecular Biophysics Program and Department of Biochemistry, University of Colorado, Boulder, CO, USA.
Molecular Biophysics Program and Department of Biochemistry, University of Colorado, Boulder, CO, USA.
Anal Biochem. 2021 Oct 15;631:114338. doi: 10.1016/j.ab.2021.114338. Epub 2021 Aug 22.
The Ras superfamily of small G proteins play central roles in diverse signaling pathways. Superfamily members act as molecular on-off switches defined by their occupancy with GTP or GDP, respectively. In vitro functional studies require loading with a hydrolysis-resistant GTP analogue to increase the on-state lifetime, as well as knowledge of fractional loading with activating and inactivating nucleotides. The present study describes a method combining elements of previous approaches with new, optimized features to analyze the bound nucleotide composition of a G protein loaded with activating (GMPPNP) or inactivating (GDP) nucleotide. After nucleotide loading, the complex is washed to remove unbound nucleotides then bound nucleotides are heat-extracted and subjected to ion-paired, reverse-phase HPLC-UV to resolve, identify and quantify the individual nucleotide components. These data enable back-calculation to the nucleotide composition and fractional activation of the original, washed G protein population prior to heat extraction. The method is highly reproducible. Application to multiple HRas preparations and mutants confirms its ability to fully extract and analyze bound nucleotides, and to resolve the fractional on- and off-state populations. Furthermore, the findings yield a novel hypothesis for the molecular disease mechanism of Ras mutations at the E63 and Y64 positions.
Ras 超家族的小分子 G 蛋白在多种信号通路中发挥着核心作用。超家族成员作为分子的开/关开关,其分别与 GTP 或 GDP 结合。体外功能研究需要加载水解抗性 GTP 类似物以增加开态寿命,以及对激活和失活核苷酸的分数加载的了解。本研究描述了一种结合先前方法的元素与新的优化功能的方法,以分析用激活(GMPPNP)或失活(GDP)核苷酸加载的 G 蛋白的结合核苷酸组成。在核苷酸加载后,将复合物洗涤以去除未结合的核苷酸,然后将结合的核苷酸进行热提取,并进行离子对、反相 HPLC-UV 分离、鉴定和定量单个核苷酸成分。这些数据可以回溯计算原始、洗涤过的 G 蛋白群体在热提取之前的核苷酸组成和分数激活。该方法具有高度可重复性。对多个 HRas 制剂和突变体的应用证实了它能够完全提取和分析结合核苷酸,并解析分数开/关状态群体的能力。此外,这些发现为 Ras 突变在 E63 和 Y64 位置的分子疾病机制提供了一个新的假设。