Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia.
Int J Mol Sci. 2024 Nov 19;25(22):12391. doi: 10.3390/ijms252212391.
Src kinase is one of the key regulators of cellular metabolism and is dysregulated in numerous diseases, including cancer, neurodegenerative diseases, and particularly Alzheimer's disease. Despite its therapeutic importance, its full-length structure has never been obtained before, as it contains an intrinsically disordered regulatory region, SH4UD. The SH4UD region is crucial for Src activation, functional dimerization, and regulation by other kinases. In this study, we used the replica exchange molecular dynamics approach with a hybrid temperature and Hamiltonian tempering to obtain the conformational ensemble of full-length Src kinase in its non-phosphorylated state and in the presence of its two key regulatory phosphorylations: pY419 and pY530. The representative structures and simulation trajectories of non-phosphorylated pY419 and pY530 Src are available in open access. We demonstrate that pY419 phosphorylation, which is associated with Src activation, enhances its motility, whereas inhibited pY530 Src preserves relatively compact conformation. This study also provides insights into how SH4UD contributes to Src substrate binding, dimerization, and autophosphorylation, highlighting the putative role of 14-RRR-16 in this process.
Src 激酶是细胞代谢的关键调节因子之一,在许多疾病中失调,包括癌症、神经退行性疾病,特别是阿尔茨海默病。尽管它具有治疗意义,但由于其包含一个固有无序的调节区域 SH4UD,因此从未获得其全长结构。SH4UD 区域对于 Src 的激活、功能二聚化以及其他激酶的调节至关重要。在这项研究中,我们使用带有混合温度和哈密顿温度调制的复制交换分子动力学方法,获得了非磷酸化状态下全长 Src 激酶及其两个关键调节磷酸化位点 pY419 和 pY530 的构象集合。非磷酸化 pY419 和 pY530 Src 的代表性结构和模拟轨迹可公开获取。我们证明了与 Src 激活相关的 pY419 磷酸化增强了其迁移性,而抑制的 pY530 Src 则保持相对紧凑的构象。这项研究还深入了解了 SH4UD 如何促进 Src 底物结合、二聚化和自身磷酸化,突出了 14-RRR-16 在这一过程中的潜在作用。