重新审视蛋白质结构背景下的亨廷顿蛋白活性和定位信号。

IF 3.1 Q3 NEUROSCIENCES
Journal of Huntington's disease Pub Date : 2024-11-01 Epub Date: 2024-11-10 DOI:10.1177/18796397241295303
Ray Truant, Rachel J Harding, Kaitlyn Neuman, Tamara Maiuri
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引用次数: 0

摘要

自2003年以来,在亨廷顿蛋白中定义了蛋白质定位信号和活性基序。由于低温电子显微镜(EM)测定蛋白质结构技术的进步,大多数亨廷顿蛋白和HAP40的分辨率为2.6 Å,尽管在亨廷顿蛋白全长的背景下,具有聚谷氨酰胺扩增的氨基端结构仍然难以确定。利用已知蛋白质结构数据库训练的神经网络算法进行蛋白质建模的最新进展,已经产生了对研究人员有用的结构预测,但需要实验验证。在这里,我们使用cryo-EM解决的结构以及以实验结构数据为中心的建模来回顾性地回顾在cryo-EM和ai支持的结构革命之前确定的亨廷顿蛋白定位信号。我们对这些模型进行了研究,并提出了关于亨廷顿蛋白变构变化的可测试假设,以及它们如何受到聚谷氨酰胺膨胀的影响。我们还将该方法扩展到另一种多谷氨酰胺疾病蛋白,ataxin-1,扩展到脊髓小脑性共济失调1型(SCA1)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Revisiting huntingtin activity and localization signals in the context of protein structure.

Protein localization signals and activity motifs have been defined within huntingtin since 2003. Advances in technology in protein structure determination by cryo-electron microscopy (EM) have led to 2.6 Å resolution structures of huntingtin and HAP40 for the majority of the protein, although structure of the amino terminus with the polyglutamine expansion remains elusive in the context of full-length huntingtin. Recent advances in protein modeling using neural network algorithms trained on a database of known protein structures has resulted in structure predictions that are useful for researchers but need experimental validation. Here, we use both structures solved by cryo-EM as well as modeling centered around experimental structural data to retrospectively revisit huntingtin protein localization signals identified prior to the cryo-EM and AI-enabled structural revolutions. We interrogate these models as well as put forward testable hypotheses of allosteric changes in huntingtin and how they could be affected by polyglutamine expansion. We also extended this methodology to another polyglutamine disease protein, ataxin-1, expanded in Spinocerebellar Ataxia Type 1 (SCA1).

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来源期刊
CiteScore
4.80
自引率
9.70%
发文量
60
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