Reductions of the Components of the Calreticulin/Calnexin Quality-Control System by Proteasome Inhibitors and Their Relevance in a Rodent Model of Parkinson's Disease
文献类型:期刊论文
作者 | Kuang, XL; Liu, F; Chen, HF; Li, YP; Liu, YM; Xiao, J; Shan, G; Li, MJ; Snider, BJ; Qu, J |
刊名 | JOURNAL OF NEUROSCIENCE RESEARCH |
出版日期 | 2014 |
卷号 | 92期号:10页码:1319-1329 |
关键词 | ubiquitin-proteasome system (UPS) unfolded protein response (UPR) chaperone calreticulin/calnexin cycle ER quality control endoplasmic reticulum stress endoplasmic reticulum-associated degradation (ERAD) Parkinson's disease |
通讯作者 | Wu, SZ (reprint author), Wenzhou Med Univ, Sch Optometry & Ophthalmol, Natl Minist Hlth, Key Lab Visual Sci, Wenzhou 325027, Zhejiang, Peoples R China.,wszlab@mail.eye.ac.cn |
英文摘要 | Evidence indicates that the ubiquitin-proteasome system and the endoplasmic retculum (ER) quality-control system work in concert to ensure that proteins are correctly folded in the ER and that misfolded proteins are retro-transported to the cytosol for degradation by proteasomes. Dysfunction of either system results in developmental abnormalities and even death in animals. This study investigates whether and how proteasome inhibition impacts the components of the calreticulin (CRT)/calnexin (CNX) glycoprotein folding machinery, a typical ER protein quality-control system, in the context of early neuronal injury. Here we report that proteasome inhibitor treatments, at nonlethal levels, reduced protein levels of CRT and ERp57 but not of CNX. These treatments increased protein levels of CRT in culture media, an effect blocked by brefeldin A, an inhibitor of protein trafficking; by contrast, ERp57 was not detected in culture media. Knockdown of CRT levels alone increased the vulnerability of SH-SY5Y, a neuronal cell line, to 6-hydroxydopamine (6-OHDA) toxicity. In a rat model of Parkinson's disease, intrastriatal 6-OHDA lesions resulted in decreased levels of CRT and ERp57 in the midbrain. These findings suggest that reduction of the components of CRT/CNX glycoprotein quality-control system may play a role in neuronal injury in Parkinson's disease and other neurodegenerative disorders associated with dysfunction of the ubiquitin-proteasome system. (C) 2014 Wiley Periodicals, Inc. |
学科主题 | Neurosciences & Neurology |
类目[WOS] | Neurosciences |
关键词[WOS] | MG132-INDUCED MITOCHONDRIAL DYSFUNCTION ; ENDOPLASMIC-RETICULUM ; HEAT-SHOCK ; PROTEIN AGGREGATION ; ALZHEIMERS-DISEASE ; SERINE RACEMASE ; GENE-EXPRESSION ; PC12 CELLS ; CALCIUM ; DEATH |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000340504500009 |
版本 | 出版稿 |
源URL | [http://202.127.25.143/handle/331003/236] |
专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
推荐引用方式 GB/T 7714 | Kuang, XL,Liu, F,Chen, HF,et al. Reductions of the Components of the Calreticulin/Calnexin Quality-Control System by Proteasome Inhibitors and Their Relevance in a Rodent Model of Parkinson's Disease[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2014,92(10):1319-1329. |
APA | Kuang, XL.,Liu, F.,Chen, HF.,Li, YP.,Liu, YM.,...&Wu, SZ.(2014).Reductions of the Components of the Calreticulin/Calnexin Quality-Control System by Proteasome Inhibitors and Their Relevance in a Rodent Model of Parkinson's Disease.JOURNAL OF NEUROSCIENCE RESEARCH,92(10),1319-1329. |
MLA | Kuang, XL,et al."Reductions of the Components of the Calreticulin/Calnexin Quality-Control System by Proteasome Inhibitors and Their Relevance in a Rodent Model of Parkinson's Disease".JOURNAL OF NEUROSCIENCE RESEARCH 92.10(2014):1319-1329. |
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