Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, India.
FEBS Lett. 2020 Sep;594(17):2894-2903. doi: 10.1002/1873-3468.13873. Epub 2020 Jul 11.
Aggregation of polyglutamine proteins is a hallmark of several neurodegenerative diseases. The 11-residue polyglutamine binding peptide Ac-SNWKWWPGIFD-am, known as QBP1, inhibits polyglutamine aggregation. Besides, a minimal 8-residue stretch in the QBP1 peptide (Ac-WKWWPGIF-am) is reported in the literature to retain this activity. Both peptides harbor a Pro-Gly dipeptide motif, a feature characteristic of potential β-turn regions. Here, we investigated whether the presence of this β-turn motif is necessary for the inhibition of huntingtin aggregation, a polyglutamine protein implicated in Huntington's disease. Using single amino acid substitutions to generate analogs that could support, introduce, or eliminate the β-turn, we show that the turn-supporting motif is essential for QBP1-mediated inhibition of huntingtin aggregation.
多聚谷氨酰胺蛋白的聚集是几种神经退行性疾病的一个标志。11 个残基的多聚谷氨酰胺结合肽 Ac-SNWKWWPGIFD-am,称为 QBP1,可抑制多聚谷氨酰胺聚集。此外,文献报道 QBP1 肽(Ac-WKWWPGIF-am)中的最小 8 个残基片段保留了这种活性。这两种肽都含有一个脯氨酸-甘氨酸二肽基序,这是潜在β-转角区域的特征。在这里,我们研究了该β-转角基序的存在是否对亨廷顿病中涉及的多聚谷氨酰胺蛋白亨廷顿蛋白聚集的抑制是否必要。使用单个氨基酸取代来生成能够支持、引入或消除β-转角的类似物,我们表明,支持转角的基序对于 QBP1 介导的亨廷顿蛋白聚集的抑制是必不可少的。