| 著者 |
門脇, 寿枝
WEKO
34447
e-Rad_Researcher
40568200
| ja |
門脇, 寿枝
宮崎大学
|
| ja-Kana |
カドワキ, ヒサエ
|
| en |
Kadowaki, Hisae
University of Miyazaki
|
Search repository
Hatta, Tomohisa
Sugiyama, Kazuma
深谷, 知宏
WEKO
30184
e-Rad_Researcher
20624323
| ja |
深谷, 知宏
宮崎大学
|
| ja-Kana |
フカヤ, トモヒロ
|
| en |
Fukaya, Tomohiro
University of Miyazaki
|
Search repository
Fujisawa, Takao
Hamano, Takashi
村尾, 直哉
WEKO
34463
e-Rad_Researcher
20773534
| ja |
村尾, 直哉
宮崎大学
|
| ja-Kana |
ムラオ, ナオヤ
|
| en |
Murao, Naoya
University of Miyazaki
|
Search repository
髙見, 恭成
WEKO
16378
e-Rad_Researcher
80236356
| ja |
髙見, 恭成
宮崎大学
|
| en |
Takami, Yasunari
University of Miyazaki
|
| ja-Kana |
タカミ, ヤスナリ
|
Search repository
三苫, 修也
WEKO
34689
e-Rad_Researcher
50911111
| ja |
三苫, 修也
宮崎大学
|
| ja-Kana |
ミトマ, シュウヤ
|
| en |
Mitoma, Shuya
University of Miyazaki
|
Search repository
Natsume, Tohru
| en |
Natsume, Tohru（Personal）
National Institute of Advanced Industrial Science and Technology
|
Search repository
佐藤, 克明
WEKO
30111
e-Rad_Researcher
40301147
| ja |
佐藤, 克明
宮崎大学
|
| ja-Kana |
サトウ, カツアキ
|
| en |
Sato, Katsuaki
University of Miyazaki
|
Search repository
Hirata, Hiromi
上地, 珠代
WEKO
9591
e-Rad_Researcher
10381104
| ja |
上地, 珠代
宮崎大学
|
| ja-Kana |
ウエチ, タマヨ
|
| en |
Uechi, Tamayo
University of Miyazaki
|
Search repository
西頭, 英起
WEKO
34317
e-Rad_Researcher
00332627
| ja |
西頭, 英起
宮崎大学
|
| ja-Kana |
ニシトウ, ヒデキ
|
| en |
Nishitoh, Hideki
University of Miyazaki
|
Search repository
|
|
内容記述 |
Disrupted proteostasis causes various degenerative diseases, and organelle homeostasis is therefore maintained by elaborate mechanisms. Endoplasmic reticulum (ER) stress-induced preemptive quality control (ERpQC) counteracts stress by reducing ER load through inhibiting the translocation of newly synthesized proteins into the ER for their rapid degradation in the cytoplasm. Here, we show that Sec61β, a translocon component, prevents the overproduction of ERpQC substrates, allowing for their efficient degradation by the proteasome. Sec61β inhibits the binding of translation initiation factor eIF4E to the mRNA 5' cap structure by recruiting E3 ligase ARIH1 and eIF4E-homologous protein 4EHP, resulting in selective translational repression of ERpQC substrates. Sec61β deficiency causes overproduction of ERpQC substrates and reduces proteasome activity, leading to cytoplasmic aggresome formation. We also show that Sec61β deficiency causes motor dysfunction in zebrafish, which is restored by exogenous ARIH1 expression. Collectively, translational repression of ERpQC substrates by the Sec61β-ARIH1 complex contributes to maintain ER and cytoplasmic proteostasis. |
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