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可增强突变型亨廷顿蛋白片段或α-突触核蛋白毒性的酵母基因。

Yeast genes that enhance the toxicity of a mutant huntingtin fragment or alpha-synuclein.

作者信息

Willingham Stephen, Outeiro Tiago Fleming, DeVit Michael J, Lindquist Susan L, Muchowski Paul J

机构信息

Department of Pharmacology, University of Washington, Seattle, WA 98195-7280, USA.

出版信息

Science. 2003 Dec 5;302(5651):1769-72. doi: 10.1126/science.1090389.

Abstract

Genome-wide screens were performed in yeast to identify genes that enhance the toxicity of a mutant huntingtin fragment or of alpha-synuclein. Of 4850 haploid mutants containing deletions of nonessential genes, 52 were identified that were sensitive to a mutant huntingtin fragment, 86 that were sensitive to alpha-synuclein, and only one mutant that was sensitive to both. Genes that enhanced toxicity of the mutant huntingtin fragment clustered in the functionally related cellular processes of response to stress, protein folding, and ubiquitin-dependent protein catabolism, whereas genes that modified alpha-synuclein toxicity clustered in the processes of lipid metabolism and vesicle-mediated transport. Genes with human orthologs were overrepresented in our screens, suggesting that we may have discovered conserved and nonoverlapping sets of cell-autonomous genes and pathways that are relevant to Huntington's disease and Parkinson's disease.

摘要

在酵母中进行了全基因组筛选,以鉴定增强突变型亨廷顿蛋白片段或α-突触核蛋白毒性的基因。在4850个含有非必需基因缺失的单倍体突变体中,鉴定出52个对突变型亨廷顿蛋白片段敏感的突变体,86个对α-突触核蛋白敏感的突变体,只有一个突变体对两者都敏感。增强突变型亨廷顿蛋白片段毒性的基因聚集在与应激反应、蛋白质折叠和泛素依赖性蛋白质分解代谢功能相关的细胞过程中,而改变α-突触核蛋白毒性的基因聚集在脂质代谢和囊泡介导的运输过程中。在我们的筛选中,具有人类直系同源基因的基因占比过高,这表明我们可能发现了与亨廷顿舞蹈病和帕金森病相关的保守且不重叠的细胞自主基因和通路集。

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