Department of Molecular and Cell Biology, University of California, Berkeley, California, USA.
California Institute for Quantitative Bioscience (QB3), University of California, Berkeley, California, USA.
Protein Sci. 2024 Jun;33(6):e5023. doi: 10.1002/pro.5023.
Oncogenic mutations can destabilize signaling proteins, resulting in increased or unregulated activity. Thus, there is considerable interest in mapping the relationship between mutations and the stability of signaling proteins, to better understand the consequences of oncogenic mutations and potentially inform the development of new therapeutics. Here, we develop a tool to study protein-kinase stability in live mammalian cells and the effects of the HSP90 chaperone system on the stability of these kinases. We determine the expression levels of protein kinases by monitoring the fluorescence of fluorescent proteins fused to those kinases, normalized to that of co-expressed reference fluorescent proteins. We used this tool to study the dependence of Src- and Raf-family kinases on the HSP90 system. We demonstrate that this sensor reports on destabilization induced by oncogenic mutations in these kinases. We also show that Src-homology 2 and Src-homology 3 domains, which are required for autoinhibition of Src-family kinases, stabilize these kinase domains in the cell. Our expression-calibrated sensor enables the facile characterization of the effects of mutations and small-molecule drugs on protein-kinase stability.
致癌突变会使信号蛋白不稳定,导致其活性增加或不受调控。因此,人们非常关注将突变与信号蛋白稳定性之间的关系进行映射,以便更好地了解致癌突变的后果,并可能为新疗法的开发提供信息。在这里,我们开发了一种工具来研究活哺乳动物细胞中蛋白激酶的稳定性,以及 HSP90 伴侣系统对这些激酶稳定性的影响。我们通过监测与这些激酶融合的荧光蛋白的荧光来确定蛋白激酶的表达水平,并将其归一化为共表达的参考荧光蛋白的荧光。我们使用该工具研究了 Src 和 Raf 家族激酶对 HSP90 系统的依赖性。我们证明该传感器可报告这些激酶中致癌突变诱导的不稳定性。我们还表明,Src 同源结构域 2 和 Src 同源结构域 3 对于 Src 家族激酶的自动抑制是必需的,它们可在细胞内稳定这些激酶结构域。我们的表达校准传感器可方便地对突变和小分子药物对蛋白激酶稳定性的影响进行特征描述。