Department of Pharmacology, Penn State College of Medicine, Hershey, United States.
Department of Biomedical Engineering, Penn State University, University Park, Hershey, United States.
Elife. 2023 Nov 9;12:RP90574. doi: 10.7554/eLife.90574.
The dysregulation of protein kinases is associated with multiple diseases due to the kinases' involvement in a variety of cell signaling pathways. Manipulating protein kinase function, by controlling the active site, is a promising therapeutic and investigative strategy to mitigate and study diseases. Kinase active sites share structural similarities, making it difficult to specifically target one kinase, and allosteric control allows specific regulation and study of kinase function without directly targeting the active site. Allosteric sites are distal to the active site but coupled via a dynamic network of inter-atomic interactions between residues in the protein. Establishing an allosteric control over a kinase requires understanding the allosteric wiring of the protein. Computational techniques offer effective and inexpensive mapping of the allosteric sites on a protein. Here, we discuss the methods to map and regulate allosteric communications in proteins, and strategies to establish control over kinase functions in live cells and organisms. Protein molecules, or 'sensors,' are engineered to function as tools to control allosteric activity of the protein as these sensors have high spatiotemporal resolution and help in understanding cell phenotypes after immediate activation or inactivation of a kinase. Traditional methods used to study protein functions, such as knockout, knockdown, or mutation, cannot offer a sufficiently high spatiotemporal resolution. We discuss the modern repertoire of tools to regulate protein kinases as we enter a new era in deciphering cellular signaling and developing novel approaches to treat diseases associated with signal dysregulation.
蛋白质激酶的失调与多种疾病有关,因为激酶参与了多种细胞信号通路。通过控制活性位点来操纵蛋白质激酶的功能是一种有前途的治疗和研究策略,可以减轻和研究疾病。激酶的活性位点具有结构相似性,因此很难特异性地靶向一种激酶,而变构调控允许对激酶功能进行特异性调节和研究,而无需直接靶向活性位点。变构位点远离活性位点,但通过蛋白质中残基之间的动态原子间相互作用网络耦合。建立对激酶的变构控制需要了解蛋白质的变构布线。计算技术为在蛋白质上进行变构位点的有效和廉价映射提供了方法。在这里,我们讨论了映射和调节蛋白质中变构通讯的方法,以及在活细胞和生物体中建立对激酶功能控制的策略。蛋白质分子,或“传感器”,被设计为控制蛋白质变构活性的工具,因为这些传感器具有高时空分辨率,并有助于在激酶的立即激活或失活后理解细胞表型。用于研究蛋白质功能的传统方法,如敲除、敲低或突变,无法提供足够高的时空分辨率。我们讨论了调控蛋白质激酶的现代工具组合,因为我们进入了一个破译细胞信号并开发治疗与信号失调相关疾病的新方法的新时代。