Burgoyne Robert D, Morgan Alan
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Crown St., Liverpool L69 3BX, UK.
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Crown St., Liverpool L69 3BX, UK.
Semin Cell Dev Biol. 2015 Apr;40:153-9. doi: 10.1016/j.semcdb.2015.03.008. Epub 2015 Mar 21.
Cysteine string protein (CSP) is a member of the DnaJ/Hsp40 family of co-chaperones that localises to neuronal synaptic vesicles. Its name derives from the possession of a string of 12-15 cysteine residues, palmitoylation of which is required for targeting to post-Golgi membranes. The DnaJ domain of CSP enables it to bind client proteins and recruit Hsc70 chaperones, thereby contributing to the maintenance of protein folding in the presynaptic compartment. Mutation of CSP in flies, worms and mice reduces lifespan and causes synaptic dysfunction and neurodegeneration. Furthermore, recent studies have revealed that the neurodegenerative disease, adult onset neuronal ceroid lipofuscinosis, is caused by mutations in the human CSPα-encoding DNAJC5 gene. Accumulating evidence suggests that the major mechanism by which CSP prevents neurodegeneration is by maintaining the conformation of SNAP-25, thereby facilitating its entry into the membrane-fusing SNARE complex. In this review, we focus on the role of CSP in preventing neurodegeneration and discuss how recent studies of this universal neuroprotective chaperone are being translated into potential novel therapeutics for neurodegenerative diseases.
半胱氨酸串珠蛋白(CSP)是定位于神经元突触小泡的辅助伴侣蛋白DnaJ/Hsp40家族的成员。它的名字来源于其拥有一串12 - 15个半胱氨酸残基,其棕榈酰化是靶向高尔基体后膜所必需的。CSP的DnaJ结构域使其能够结合客户蛋白并募集Hsc70伴侣蛋白,从而有助于维持突触前区室中蛋白质的折叠。果蝇、蠕虫和小鼠中CSP的突变会缩短寿命,并导致突触功能障碍和神经退行性变。此外,最近的研究表明,神经退行性疾病成人型神经元蜡样脂褐质沉积症是由人类编码CSPα的DNAJC5基因突变引起的。越来越多的证据表明,CSP预防神经退行性变的主要机制是维持SNAP - 25的构象,从而促进其进入膜融合SNARE复合体。在这篇综述中,我们聚焦于CSP在预防神经退行性变中的作用,并讨论对这种通用神经保护伴侣蛋白的最新研究如何转化为神经退行性疾病潜在的新型治疗方法。