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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Increased susceptibility of cytoplasmic over nuclear polyglutamine aggregates to autophagic degradation
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Increased susceptibility of cytoplasmic over nuclear polyglutamine aggregates to autophagic degradation

机译：细胞质对核聚谷氨酰胺聚集体的自噬降解敏感性增加

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摘要

CNS neurons are endowed with the ability to recover from cytotoxic insults associated with the accumulation of proteinaceous aggregates in mouse models of polyglutamine disease, but the cellular mechanism underlying this phenomenon is unknown. Here, we show that autophagy is essential for the elimination of aggregated forms of mutant huntingtin and ataxin-1 from the cytoplasmic but not nuclear compartments. Human orthologs of yeast autophagy genes, molecular determinants of autophagic vacuole formation, are recruited to cytoplasmic but not nuclear inclusion bodies in vitro and in vivo. These data indicate that autophagy is a critical component of the cellular clearance of toxic protein aggregates and may help to explain why protein aggregates are more toxic when directed to the nucleus.
机译：中枢神经系统神经元具有从与聚谷氨酰胺疾病的小鼠模型中的蛋白质聚集体积累相关的细胞毒性损伤中恢复的能力，但这种现象的细胞机制尚不清楚。在这里，我们显示自噬对于从细胞质而不是核区室消除突变型亨廷顿蛋白和共青素-1的聚集形式至关重要。酵母自噬基因的人类直系同源物，自噬泡形成的分子决定因素，在体外和体内被募集到细胞质而不是核包涵体。这些数据表明自噬是有毒蛋白质聚集体细胞清除的重要组成部分，并可能有助于解释为什么蛋白质聚集体直接进入细胞核时毒性更大。

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