Molecular sensing using model membranes

我们已经（i）表明淀粉样蛋白β（Ab）以物种依赖性和膜组成的方式与膜相互作用。它们引起膜的转化、破裂和粘性。这些可能有助于了解毒性机制;（ii）研究了胆固醇氧化如何影响膜动力学，表明温度升高使氧化膜更流畅。我们用生物细胞也有类似的发现。研究结果是有用的澄清胆固醇的影响，在抗体诱导的毒性;（iv）氧化膜增强抗体的协会与膜;（v）潜在的神经保护剂相互作用的膜的结构依赖性的方式，因为他们的能力，以抑制抗体聚集。在官能团水平上揭示这些化合物的重要性打开了定制设计潜在生物活性药物候选物的关键。我们研制了一种抗体免疫传感器芯片。

We have (i) shown that amyloid beta (Ab) interacts with membranes in a species-dependent and membrane composition manner. They cause membrane transformation, breach and viscosity. These may contribute towards understanding toxicity mechanisms; (ii) studied how oxidation of cholesterol influences membrane dynamics, demonstrating that temperature increase renders oxidized membranes more fluid. We have similar findings using biological cells. The findings are useful for clarifying the impact of cholesterol in Ab-induced toxicity; (iv) oxidized membranes enhance Ab's association with membranes; (v) potential neuro-protective agents interact with membranes in a structure-dependent manner as does their ability to inhibit Ab aggregation. Unraveling the importance of these compounds, at a functional group level opens the key to tailored design of potential bioactive drug candidates. We have developed an immunosensor chip for Ab.