Peters Judith, Rittger Andrea, Weisner Rebecca, Knabbe Johannes, Zunke Friederike, Rothaug Michelle, Damme Markus, Berkovic Samuel F, Blanz Judith, Saftig Paul, Schwake Michael
Institut für Biochemie, Christian-Albrechts-Universität zu Kiel, Olshausenstrasse 40, D-24098 Kiel, Germany.
Epilepsy Research Centre, Department of Medicine, University of Melbourne, Austin Health, Heidelberg 3084, Australia.
Biochem Biophys Res Commun. 2015 Feb 13;457(3):334-40. doi: 10.1016/j.bbrc.2014.12.111. Epub 2015 Jan 7.
The lysosomal integral membrane protein type-2 (LIMP-2/SCARB2) has been identified as a receptor for enterovirus 71 uptake and mannose-6-phosphate-independent lysosomal trafficking of the acid hydrolase β-glucocerebrosidase. Here we show that LIMP-2 undergoes proteolytic cleavage mediated by lysosomal cysteine proteases. Heterologous expression and in vitro studies suggest that cathepsin-F is mainly responsible for the lysosomal processing of wild-type LIMP-2. Furthermore, examination of purified lysosomes revealed that LIMP-2 undergoes proteolysis in vivo. Mutations in the gene encoding cathepsin-F (CTSF) have recently been associated with type-B-Kufs-disease, an adult form of neuronal ceroid-lipofuscinosis. In this study we show that disease-causing cathepsin-F mutants fail to cleave LIMP-2. Our findings provide evidence that LIMP-2 represents an in vivo substrate of cathepsin-F with relevance for understanding the pathophysiology of type-B-Kufs-disease.
溶酶体整合膜蛋白2型(LIMP-2/SCARB2)已被确定为肠道病毒71摄取的受体以及酸性水解酶β-葡萄糖脑苷脂酶不依赖甘露糖-6-磷酸的溶酶体运输受体。在此我们表明,LIMP-2会经历由溶酶体半胱氨酸蛋白酶介导的蛋白水解切割。异源表达和体外研究表明,组织蛋白酶F主要负责野生型LIMP-2的溶酶体加工过程。此外,对纯化的溶酶体进行检测发现,LIMP-2在体内会发生蛋白水解。编码组织蛋白酶F(CTSF)的基因突变最近与B型库夫斯病相关,这是一种成人形式的神经元蜡样脂褐质沉积症。在本研究中,我们表明致病的组织蛋白酶F突变体无法切割LIMP-2。我们的研究结果提供了证据,表明LIMP-2是组织蛋白酶F的一种体内底物,这对于理解B型库夫斯病的病理生理学具有重要意义。