Gambin Yann, Polinkovsky Mark, Francois Bill, Giles Nichole, Bhumkar Akshay, Sierecki Emma
EMBL Australia Node in Single Molecule Sciences, School of Medical Science, the University of New South Wales, Sydney, NSW 2052, Australia.
Int J Mol Sci. 2016 Apr 30;17(5):655. doi: 10.3390/ijms17050655.
Protein self-association is a key feature that can modulate the physiological role of proteins or lead to deleterious effects when uncontrolled. Protein oligomerization is a simple way to modify the activity of a protein, as the modulation of binding interfaces allows for self-activation or inhibition, or variation in the selectivity of binding partners. As such, dimerization and higher order oligomerization is a common feature in signaling proteins, for example, and more than 70% of enzymes have the potential to self-associate. On the other hand, protein aggregation can overcome the regulatory mechanisms of the cell and can have disastrous physiological effects. This is the case in a number of neurodegenerative diseases, where proteins, due to mutation or dysregulation later in life, start polymerizing and often fibrillate, leading to the creation of protein inclusion bodies in cells. Dimerization, well-defined oligomerization and random aggregation are often difficult to differentiate and characterize experimentally. Single molecule "counting" methods are particularly well suited to the study of self-oligomerization as they allow observation and quantification of behaviors in heterogeneous conditions. However, the extreme dilution of samples often causes weak complexes to dissociate, and rare events can be overlooked. Here, we discuss a straightforward alternative where the principles of single molecule detection are used at higher protein concentrations to quantify oligomers and aggregates in a background of monomers. We propose a practical guide for the use of confocal spectroscopy to quantify protein oligomerization status and also discuss about its use in monitoring changes in protein aggregation in drug screening assays.
蛋白质自缔合是一个关键特性,它可以调节蛋白质的生理作用,但若不受控制则会导致有害影响。蛋白质寡聚化是改变蛋白质活性的一种简单方式,因为结合界面的调节允许自我激活或抑制,或者改变结合伴侣的选择性。例如,二聚化和更高阶的寡聚化是信号蛋白的常见特征,超过70%的酶具有自缔合的潜力。另一方面,蛋白质聚集可以克服细胞的调节机制,并可能产生灾难性的生理影响。许多神经退行性疾病就是这种情况,由于蛋白质在生命后期发生突变或失调,开始聚合并经常形成纤维状,导致细胞中形成蛋白质包涵体。二聚化、明确的寡聚化和随机聚集通常很难通过实验进行区分和表征。单分子“计数”方法特别适合于自寡聚化的研究,因为它们允许在异质条件下观察和量化行为。然而,样品的极度稀释往往会导致弱复合物解离,罕见事件可能会被忽视。在这里,我们讨论一种直接的替代方法,即在较高的蛋白质浓度下使用单分子检测原理来量化单体背景中的寡聚物和聚集体。我们提出了一份使用共聚焦光谱法定量蛋白质寡聚化状态的实用指南,并讨论了其在药物筛选试验中监测蛋白质聚集变化的用途。