Nicotinic acetylcholine receptor signaling regulates inositol-requiring enzyme 1α activation to protect β-cells against terminal unfolded protein response under irremediable endoplasmic reticulum stress.,Journal of Diabetes Investigation

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Nicotinic acetylcholine receptor signaling regulates inositol-requiring enzyme 1α activation to protect β-cells against terminal unfolded protein response under irremediable endoplasmic reticulum stress.
Journal of Diabetes Investigation ( IF 3.1 ) Pub Date : 2020-02-17 , DOI: 10.1111/jdi.13211
Tatsuya Ishibashi ₁ , Shuhei Morita ₁ , Shohei Kishimoto ₁ , Shinsuke Uraki ₁ , Ken Takeshima ₁ , Yasushi Furukawa ₁ , Hidefumi Inaba ₁ , Hiroyuki Ariyasu ₁ , Hiroshi Iwakura ₁ , Hiroto Furuta ₁ , Masahiro Nishi ₁ , Feroz R Papa _{2,

3,

4} , Takashi Akamizu ₁

Affiliation

Under irremediable endoplasmic reticulum (ER) stress, hyperactivated inositol‐requiring enzyme 1α (IRE1α) triggers the terminal unfolded protein response (T‐UPR), causing crucial cell dysfunction and apoptosis. We hypothesized that nicotinic acetylcholine receptor (nAChR) signaling regulates IRE1α activation to protect β‐cells from the T‐UPR under ER stress.

中文翻译：

烟碱乙酰胆碱受体信号传导调节肌醇需求酶 1α 激活，以保护 β 细胞在不可修复的内质网应激下免受终末未折叠蛋白反应。

在不可挽回的内质网 (ER) 应激下，过度活化的肌醇需求酶 1α (IRE1α) 会触发末端未折叠蛋白反应 (T-UPR)，导致关键的细胞功能障碍和细胞凋亡。我们假设烟碱乙酰胆碱受体 (nAChR) 信号传导调节 IRE1α 激活，以保护 β 细胞免受 ER 应激下 T-UPR 的影响。

更新日期：2020-02-17

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