| Item type |
文献 / Documents(1) |
| 公開日 |
2021-08-11 |
| アクセス権 |
|
|
アクセス権 |
open access |
| 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 |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1016/j.isci.2020.101299 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1016/j.isci.2020.101299 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Enhanced O-GlcNAcylation Mediates Cytoprotection under Proteasome Impairment by Promoting Proteasome Turnover in Cancer Cells |
|
言語 |
en |
| 著者 |
ハシモト, エイイチ
オクノ, ショウタ
ヒラヤマ, ショウシロウ
アラタ, ヨシユキ
ゴトウ, ツヨシ
小迫, 英尊
ハマザキ, ジュン
ムラタ, シゲオ
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
The proteasome is a therapeutic target in cancer, but resistance to proteasome inhibitors often develops owing to the induction of compensatory pathways. Through a genome-wide siRNA screen combined with RNA sequencing analysis, we identified hexokinase and downstream O-GlcNAcylation as cell survival factors under proteasome impairment. The inhibition of O-GlcNAcylation synergistically induced massive cell death in combination with proteasome inhibition. We further demonstrated that O-GlcNAcylation was indispensable for maintaining proteasome activity by enhancing biogenesis as well as proteasome degradation in a manner independent of Nrf1, a well-known compensatory transcription factor that upregulates proteasome gene expression. Our results identify a pathway that maintains proteasome function under proteasome impairment, providing potential targets for cancer therapy. |
|
言語 |
en |
| 書誌情報 |
en : iScience
巻 23,
号 7,
p. 101299,
発行日 2020-07-24
|
| 収録物ID |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
25890042 |
| 出版者 |
|
|
出版者 |
Elsevier |
|
言語 |
en |
| 権利情報 |
|
|
言語 |
en |
|
権利情報 |
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
| EID |
|
|
識別子 |
370220 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
isci_23_7_101299.pdf (28.4 MB)
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