| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2010-08-18 |
| タイトル |
|
|
タイトル |
＜Symposium III＞Nubopathies : NUB1-related neurodegenerative diseases |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
Parkinson’s disease |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
NUB1 |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
NEDD8 |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
ubiquitin |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
proteasome |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 著者 |
Tanji, Kunikazu
Mori, Fumiaki
Wakabayashi, Koichi
|
| 著者(ヨミ) |
|
|
|
識別子Scheme |
WEKO |
|
|
識別子 |
12447 |
|
|
姓名 |
タンジ, クニカズ |
| 著者(ヨミ) |
|
|
|
識別子Scheme |
WEKO |
|
|
識別子 |
9400 |
|
|
姓名 |
モリ, フミアキ |
| 著者(ヨミ) |
|
|
|
識別子Scheme |
WEKO |
|
|
識別子 |
9399 |
|
|
姓名 |
ワカバヤシ, コウイチ |
| 著者別名 |
|
|
|
識別子Scheme |
WEKO |
|
|
識別子 |
11869 |
|
|
識別子Scheme |
研究者総覧 |
|
|
識別子URI |
http://hue2.jm.hirosaki-u.ac.jp/html/314_ja.html |
|
|
識別子 |
314 |
|
|
姓名 |
Tanji, Kunikazu |
| 著者別名 |
|
|
|
識別子Scheme |
WEKO |
|
|
識別子 |
9404 |
|
|
姓名 |
Mori, Fumiaki |
| 著者別名 |
|
|
|
識別子Scheme |
WEKO |
|
|
識別子 |
9403 |
|
|
姓名 |
Wakabayashi, Koichi |
| 著者所属 |
|
|
値 |
Department of Neuropathology, Hirosaki University School of Medicine |
| 著者所属 |
|
|
値 |
Department of Neuropathology, Hirosaki University School of Medicine |
| 著者所属 |
|
|
値 |
Department of Neuropathology, Hirosaki University School of Medicine |
| 著者所属 |
|
|
値 |
Center for Molecular Chaperone, Medical College of Georgia |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
NEDD8 ultimate buster-1 （NUB1） is a potent down-regulator of the ubiquitin-like protein NEDD8, because it directly interacts with NEDD8 and targets it and its conjugates to the 26S proteasome for proteolytic degradation. Recently, we found that NUB1 physically interacts with synphilin-1 through its NEDD8-binding site, implying that NUB1 also targets synphilin-1 to the 26S proteasome for proteolytic degradation. Synphilin-1 is an α-synuclein-interacting protein and is a major component of inclusion bodies found in the brains of patients with neurodegenerative α-synucleinopathies, including Parkinson’s disease. In our recent studies, we immunostained sections of brains from patients with Parkinson’s disease and other α-synucleinopathies and demonstrated that NUB1, as well as synphilin-1, accumulates in the inclusion bodies. To defi ne the role of NUB1 in the formation of these inclusion bodies, we performed a co-transfection assay using cultured HEK293 cells. This assay showed that NUB1 suppresses the formation of synphilin-1-positive inclusions. Further biochemical assays revealed that NUB1 overexpression leads to the proteasomal degradation of synphilin-1. These results and our previous observations suggest that NUB1 indeed targets synphilin-1 to the proteasome for its effi cient degradation, which, because of the resultant reduction in synphilin-1, suppresses the formation of synphilin-1-positive inclusions. In addition to these basic science aspects, our fi ndings on NUB1 have two important bearings clinically. First, they suggest that NUB1 could serve as a neuropathological marker in patients with α-synucleinopathies because it is strongly accumulated with synphilin-1 in the inclusions of their brain cells. Second, they suggest that NUB1 could be a potential therapeutic target for α-synucleinopathies. |
| 引用 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
弘前医学. 61(Suppl.), 2010, p.S89-96 |
| 書誌情報 |
弘前医学
巻 61,
号 Supplement,
p. S89-S96,
発行日 2010-07-08
|
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0439-1721 |
| 書誌レコードID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AN00211444 |
| 著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 日本十進分類法 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
| NIIサブジェクト |
|
|
主題Scheme |
Other |
|
主題 |
医学 |
| 出版者 |
|
|
出版者 |
弘前大学大学院医学研究科・弘前医学会 |
| 資源タイプ |
|
|
値 |
Article |
HirosakiMedJ_61_S89.pdf (193.8 kB)
