Electrostatic Complementarity Drives Amyloid/Nucleic Acid Co-Assembly
Electrostatic Complementarity Drives Amyloid/Nucleic Acid Co-Assembly
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DOI：
10.1002/anie.201907661
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发表时间：
2019-11-14
影响因子：
16.6
通讯作者：
Lynn, David G.
中科院分区：
文献类型：
--
作者：
Rha, Allisandra K.;Das, Dibyendu;Lynn, David G.
与神经退行性疾病相关的蛋白斑块含有许多生物聚合物，包括多阴离子、糖胺聚糖和核酸。聚阴离子诱导的淀粉样蛋白纤颤与疾病病因有关，但淀粉样蛋白/核酸共组装的结构模型仍然有限。在这里，我们约束核酸/肽与利用静电互补的模型肽的相互作用，并定义了一种新的淀粉样蛋白/核酸共组装。该结构为核酸/淀粉样蛋白共组装提供了模型，并深入了解了淀粉样蛋白模板组装中涉及的能量决定因素。
Proteinaceous plaques associated with neurodegenerative diseases contain many biopolymers including the polyanions glycosaminoglycans and nucleic acids. Polyanion-induced amyloid fibrillation has been implicated in disease etiology, but structural models for amyloid/nucleic acid co-assemblies remain limited. Here we constrain nucleic acid/peptide interactions with model peptides that exploit electrostatic complementarity and define a novel amyloid/nucleic acid co-assembly. The structure provides a model for nucleic acid/amyloid co-assembly as well as insight into the energetic determinants involved in templating amyloid assembly.