未折叠蛋白反应
医学
内质网
信号转导
XBP1型
转录因子
蛋白激酶A
激酶
平衡
细胞生物学
生物化学
基因
生物
核糖核酸
RNA剪接
作者
Fı̇rdevs Sak,Fatma Şengül,Hüsamettin Vatansev
出处
期刊:Metabolic Syndrome and Related Disorders
[Mary Ann Liebert]
日期:2024-04-26
卷期号:22 (7): 487-493
被引量:3
标识
DOI:10.1089/met.2024.0013
摘要
The endoplasmic reticulum (ER), the center of protein folding, also controls the cell's life-and-death signaling mechanisms. ER stress caused by unfolded or misfolded proteins leads to the activation of the unfolded protein response (UPR) in the cell. The UPR utilizes three main signaling pathways to restore disrupted ER homeostasis. These signaling pathways are protein kinase R-like endoplasmic reticulum kinase, inositol-requiring enzyme 1, and activating transcription factor 6. Studies have reported that ER stress (ERS) plays a role in the pathogenesis of metabolic disorders such as diabetes, obesity, atherosclerosis, and nonalcoholic liver disease. This review will briefly discuss the ERS response in these metabolic diseases.
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