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缺乏抗肌萎缩蛋白相关蛋白和抗肌萎缩蛋白的小鼠作为杜氏肌营养不良症的模型。

Utrophin-dystrophin-deficient mice as a model for Duchenne muscular dystrophy.

作者信息

Deconinck A E, Rafael J A, Skinner J A, Brown S C, Potter A C, Metzinger L, Watt D J, Dickson J G, Tinsley J M, Davies K E

机构信息

Department of Biochemistry, University of Oxford, United Kingdom.

出版信息

Cell. 1997 Aug 22;90(4):717-27. doi: 10.1016/s0092-8674(00)80532-2.

Abstract

The absence of dystrophin at the muscle membrane leads to Duchenne muscular dystrophy (DMD), a severe muscle-wasting disease that is inevitably fatal in early adulthood. In contrast, dystrophin-deficient mdx mice appear physically normal despite their underlying muscle pathology. We describe mice deficient for both dystrophin and the dystrophin-related protein utrophin. These mice show many signs typical of DMD in humans: they show severe progressive muscular dystrophy that results in premature death, they have ultrastructural neuromuscular and myotendinous junction abnormalities, and they aberrantly coexpress myosin heavy chain isoforms within a fiber. The data suggest that utrophin and dystrophin have complementing roles in normal functional or developmental pathways in muscle. Detailed study of these mice should provide novel insights into the pathogenesis of DMD and provide an improved model for rapid evaluation of gene therapy strategies.

摘要

肌膜上缺乏抗肌萎缩蛋白会导致杜氏肌营养不良症(DMD),这是一种严重的肌肉萎缩疾病,在成年早期必然致命。相比之下,缺乏抗肌萎缩蛋白的mdx小鼠尽管存在潜在的肌肉病理状况,但身体外观正常。我们描述了同时缺乏抗肌萎缩蛋白和与抗肌萎缩蛋白相关的蛋白质——肌养蛋白的小鼠。这些小鼠表现出许多人类DMD典型的症状:它们表现出严重的进行性肌营养不良,导致过早死亡,存在超微结构的神经肌肉和肌腱连接异常,并且在肌纤维内异常共表达肌球蛋白重链异构体。数据表明,肌养蛋白和抗肌萎缩蛋白在肌肉正常功能或发育途径中具有互补作用。对这些小鼠的详细研究应能为DMD的发病机制提供新的见解,并为快速评估基因治疗策略提供更好的模型。

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