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丰富的鱼蛋白能抑制α-突触核蛋白的淀粉样形成。

Abundant fish protein inhibits α-synuclein amyloid formation.

机构信息

Department of Biology and Biological Engineering, Chalmers University of Technology, 412 96, Gothenburg, Sweden.

出版信息

Sci Rep. 2018 Apr 3;8(1):5465. doi: 10.1038/s41598-018-23850-0.

Abstract

The most common allergen in fish, the highly-abundant protein β-parvalbumin, forms amyloid structures as a way to avoid gastrointestinal degradation and transit to the blood. In humans, the same amyloid structures are mostly associated with neurodegenerative disorders such as Alzheimer's and Parkinson's. We here assessed a putative connection between these amyloids using recombinant Atlantic cod β-parvalbumin and the key amyloidogenic protein in Parkinson's disease, α-synuclein. Using a set of in vitro biophysical methods, we discovered that β-parvalbumin readily inhibits amyloid formation of α-synuclein. The underlying mechanism was found to involve α-synuclein binding to the surface of β-parvalbumin amyloid fibers. In addition to being a new amyloid inhibition mechanism, the data suggest that health benefits of fish may be explained in part by cross-reaction of β-parvalbumin with human amyloidogenic proteins.

摘要

鱼类中最常见的过敏原是高度丰富的蛋白质β-副肌球蛋白,它形成淀粉样结构是为了避免胃肠道降解并转移到血液中。在人类中,同样的淀粉样结构主要与神经退行性疾病如阿尔茨海默病和帕金森病有关。在这里,我们使用重组大西洋鳕鱼β-副肌球蛋白和帕金森病中的关键淀粉样蛋白α-突触核蛋白评估了这些淀粉样蛋白之间的潜在联系。使用一系列体外生物物理方法,我们发现β-副肌球蛋白可以轻易抑制α-突触核蛋白的淀粉样形成。研究发现,其潜在机制涉及α-突触核蛋白与β-副肌球蛋白淀粉样纤维表面的结合。除了作为一种新的淀粉样抑制机制外,该数据还表明鱼类的健康益处可能部分归因于β-副肌球蛋白与人淀粉样蛋白的交叉反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ff/5882657/36b9148944b5/41598_2018_23850_Fig1_HTML.jpg

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