Quantum defects in single-walled carbon nanotubes promote exciton localization, which enables potential applications in biodevices and quantum light sources. However, the effects of local electric fields on the emissive energy states of quantum defects and how they can be controlled are unexplored. Here, we investigate quantum defect sensitization by engineering an intrinsically disordered protein to undergo a phase change at a quantum defect site. We designed a supercharged single-chain antibody fragment (scFv) to enable a full ligand-induced folding transition from an intrinsically disordered state to a compact folded state in the presence of a cytokine. The supercharged scFv was conjugated to a quantum defect to induce a substantial local electric change upon ligand binding. Employing the detection of a proinflammatory biomarker, interleukin-6, as a representative model system, supercharged scFv-coupled quantum defects exhibited robust fluorescence wavelength shifts concomitant with the protein folding transition. Quantum chemical simulations suggest that the quantum defects amplify the optical response to the localization of charges produced upon the antigen-induced folding of the proteins, which is difficult to achieve in unmodified nanotubes. These findings portend new approaches to modulate quantum defect emission for biomarker sensing and protein biophysics and to engineer proteins to modulate binding signal transduction.

中文翻译：

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通过相变增压抗体片段进行量子缺陷敏化

单壁碳纳米管中的量子缺陷促进激子局域化，这使得其在生物器件和量子光源中具有潜在的应用。然而，局域电场对量子缺陷发射能态的影响以及如何控制它们尚未得到探索。在这里，我们通过设计本质上无序的蛋白质在量子缺陷位点经历相变来研究量子缺陷敏化。我们设计了一种增压单链抗体片段（scFv），以在细胞因子存在的情况下实现从本质上无序状态到紧凑折叠状态的完全配体诱导的折叠转变。超荷电的 scFv 与量子缺陷缀合，在配体结合时诱导显着的局部电变化。采用促炎生物标志物 IL-6 的检测作为代表性模型系统，增压 scFv 耦合量子缺陷表现出伴随蛋白质折叠转变的强大荧光波长变化。量子化学模拟表明，量子缺陷放大了对抗原诱导的蛋白质折叠时产生的电荷定位的光学响应，这在未修饰的纳米管中很难实现。这些发现预示着调节生物标志物传感和蛋白质生物物理学的量子缺陷发射以及工程蛋白质以调节结合信号转导的新方法。