Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김태수 | * |
dc.date.accessioned | 2017-10-27T11:45:27Z | - |
dc.date.available | 2017-10-27T11:45:27Z | - |
dc.date.issued | 2017 | * |
dc.identifier.issn | 2211-1247 | * |
dc.identifier.other | OAK-20976 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/237207 | - |
dc.description.abstract | Dendrite aberration is a common feature of neurode-generative diseases caused by protein toxicity, but the underlying mechanisms remain largely elusive. Here, we show that nuclear polyglutamine (polyQ) toxicity resulted in defective terminal dendrite elongation accompanied by a loss of Golgi outposts (GOPs) and a decreased supply of plasma membrane (PM) in Drosophila class IV dendritic arborization (da) (C4 da) neurons. mRNA sequencing revealed that genes downregulated by polyQ proteins included many secretory pathway-related genes, including COPII genes regulating GOP synthesis. Transcription factor enrichment analysis identified CREB3L1/CrebA, which regulates COPII gene expression. CrebA overexpression in C4 da neurons restores the dysregulation of COPII genes, GOP synthesis, and PM supply. Chromatin immunoprecipitation (ChIP)-PCR revealed that CrebA expression is regulated by CREB-binding protein (CBP), which is sequestered by polyQ proteins. Furthermore, co-overexpression of CrebA and Rac1 synergistically restores the polyQ-induced dendrite pathology. Collectively, our results suggest that GOPs impaired by polyQ proteins contribute to dendrite pathology through the CBP-CrebA-COPII pathway. | * |
dc.language | English | * |
dc.publisher | CELL PRESS | * |
dc.title | Golgi Outpost Synthesis Impaired by Toxic Polyglutamine Proteins Contributes to Dendritic Pathology in Neurons | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 20 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 356 | * |
dc.relation.lastpage | 369 | * |
dc.relation.journaltitle | CELL REPORTS | * |
dc.identifier.doi | 10.1016/j.celrep.2017.06.059 | * |
dc.identifier.wosid | WOS:000405198100008 | * |
dc.identifier.scopusid | 2-s2.0-85022035025 | * |
dc.author.google | Chung, Chang Geon | * |
dc.author.google | Kwon, Min Jee | * |
dc.author.google | Jeon, Keun Hye | * |
dc.author.google | Hyeon, Do Young | * |
dc.author.google | Han, Myeong Hoon | * |
dc.author.google | Park, Jeong Hyang | * |
dc.author.google | Cha, In Jun | * |
dc.author.google | Cho, Jae Ho | * |
dc.author.google | Kim, Kunhyung | * |
dc.author.google | Rho, Sangchul | * |
dc.author.google | Kim, Gyu Ree | * |
dc.author.google | Jeong, Hyobin | * |
dc.author.google | Lee, Jae Won | * |
dc.author.google | Kim, TaeSoo | * |
dc.author.google | Kim, Keetae | * |
dc.author.google | Kim, Kwang Pyo | * |
dc.author.google | Ehlers, Michael D. | * |
dc.author.google | Hwang, Daehee | * |
dc.author.google | Lee, Sung Bae | * |
dc.contributor.scopusid | 김태수(57223774706) | * |
dc.date.modifydate | 20240429111322 | * |