Effect of molecular chaperone on misfolding protein aggregation

蛋白质错误折叠疾病，如阿尔茨海默病(AD)，是由错误折叠的蛋白质聚集体引起的，导致分子应激和干扰细胞功能。我们检测了分子伴侣预折叠蛋白(PFD)对分别导致AD和Huntington病的淀粉样β蛋白和聚谷氨酰胺蛋白聚集的影响。我们发现，PFD在体外可以抑制它们的聚集。

Protein misfolding disease, such as Alzheimer's' disease(AD), is caused by misfolded protein aggregates that induce molecular stress and interfere with cellular function. We examined effect of molecular chaperone prefoldin(PFD) on aggregation of amyloid beta and poly glutamine protein that cause AD and Huntington disease, respectively. We found that PFD could inhibit their aggregation in vitro.