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一种基于图像的新型高通量筛选检测方法发现了成人多糖体病的治疗候选药物。

A novel image-based high-throughput screening assay discovers therapeutic candidates for adult polyglucosan body disease.

作者信息

Solmesky Leonardo J, Khazanov Netaly, Senderowitz Hanoch, Wang Peixiang, Minassian Berge A, Ferreira Igor M, Yue Wyatt W, Lossos Alexander, Weil Miguel, Kakhlon Or

机构信息

Cell Screening Facility for Personalized Medicine, Department of Cell Research and Immunology, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.

Department of Chemistry, Bar Ilan University, Ramat Gan, Israel.

出版信息

Biochem J. 2017 Sep 28;474(20):3403-3420. doi: 10.1042/BCJ20170469.

Abstract

Glycogen storage disorders (GSDs) are caused by excessive accumulation of glycogen. Some GSDs [adult polyglucosan (PG) body disease (APBD), and Tarui and Lafora diseases] are caused by intracellular accumulation of insoluble inclusions, called PG bodies (PBs), which are chiefly composed of malconstructed glycogen. We developed an APBD patient skin fibroblast cell-based assay for PB identification, where the bodies are identified as amylase-resistant periodic acid-Schiff's-stained structures, and quantified. We screened the DIVERSet CL 10 084 compound library using this assay in high-throughput format and discovered 11 dose-dependent and 8 non-dose-dependent PB-reducing hits. Approximately 70% of the hits appear to act through reducing glycogen synthase (GS) activity, which can elongate glycogen chains and presumably promote PB generation. Some of these GS inhibiting hits were also computationally predicted to be similar to drugs interacting with the GS activator protein phosphatase 1. Our work paves the way to discovering medications for the treatment of PB-involving GSD, which are extremely severe or fatal disorders.

摘要

糖原贮积病(GSDs)是由糖原过度积累引起的。一些糖原贮积病[成人多聚葡萄糖(PG)体病(APBD)、Tarui病和Lafora病]是由细胞内不溶性内含物(称为PG体,主要由结构异常的糖原组成)的积累引起的。我们开发了一种基于APBD患者皮肤成纤维细胞的PG体鉴定检测方法,其中PG体被鉴定为抗淀粉酶的过碘酸希夫氏染色结构,并进行定量。我们使用该检测方法以高通量形式筛选了DIVERSet CL 10084化合物库,发现了11个剂量依赖性和8个非剂量依赖性减少PG体的活性成分。大约70%的活性成分似乎通过降低糖原合酶(GS)活性起作用,GS可以延长糖原链并可能促进PG体的产生。其中一些抑制GS的活性成分在计算机模拟中也被预测与与GS激活蛋白磷酸酶1相互作用的药物相似。我们的工作为发现治疗涉及PG体的糖原贮积病的药物铺平了道路,这些疾病极其严重或致命。

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