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犬类CLN5基因的突变会导致边境牧羊犬患上神经元蜡样脂褐质沉积症。

A mutation in canine CLN5 causes neuronal ceroid lipofuscinosis in Border collie dogs.

作者信息

Melville Scott A, Wilson Carmen L, Chiang Chiu S, Studdert Virginia P, Lingaas Frode, Wilton Alan N

机构信息

School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia.

出版信息

Genomics. 2005 Sep;86(3):287-94. doi: 10.1016/j.ygeno.2005.06.005.

Abstract

Neuronal ceroid lipofuscinosis (NCL) is a neurodegenerative disease found in Border collie dogs, humans, and other animals. Disease gene studies in humans and animals provided candidates for the NCL gene in Border collies. A combination of linkage analysis and comparative genomics localized the gene to CFA22 in an area syntenic to HSA13q that contains the CLN5 gene responsible for the Finnish variant of human late infantile NCL. Sequencing of CLN5 revealed a nonsense mutation (Q206X) within exon 4 that correlated with NCL in Border collies. This truncation mutation should result in a protein product of a size similar to that of some mutations identified in human CLN5 and therefore the Border collie may make a good model for human NCL. A simple test was developed to enable screening of the Border collie population for carriers so the disease can be eliminated as a problem in the breed.

摘要

神经元蜡样脂褐质沉积症(NCL)是一种在边境牧羊犬、人类及其他动物中发现的神经退行性疾病。对人类和动物的疾病基因研究为边境牧羊犬的NCL基因提供了候选基因。连锁分析和比较基因组学相结合,将该基因定位到犬22号染色体(CFA22)上与人类13号染色体长臂(HSA13q)同线的区域,该区域包含导致人类晚发性婴儿型NCL芬兰变种的CLN5基因。CLN5测序显示外显子4内存在一个无义突变(Q206X),这与边境牧羊犬的NCL相关。这种截短突变应会产生一种大小与人CLN5中鉴定出一些突变类似的蛋白质产物,因此边境牧羊犬可能成为人类NCL的良好模型。开发了一种简单测试方法,用于在边境牧羊犬群体中筛查携带者,以便在该品种中消除这种疾病问题。

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