PDF(Pubmed)
Abstract：
Alteration in the physiological state of the endoplasmic reticulum (ER) leads to the specific response known as unfolded protein response (UPR) or ER stress response. The UPR is driven by three sensor proteins, namely: Inositol-Requiring Enzyme 1, Protein Kinase RNA-like ER kinase and Activating Transcription Factor 6 to restore ER homeostasis. Pathogenic infection can initiate UPR activation; some pathogens can subvert the UPR to promote their survival and replication. Many intracellular pathogens, including Leishmania, can interact and hijack ER for their survival and replication, triggering ER stress and subsequently ER stress response. This review aims to provide a comprehensive overview of the ER stress response in infections with the Leishmania species.
摘要：
内质网(ER)的生理状态的改变导致称为未折叠蛋白应答(UPR)或ER应激反应的特异性应答。UPR由三种传感器蛋白驱动，即：肌醇需求酶1，蛋白激酶RNA样ER激酶和激活转录因子6以恢复ER稳态。病原体感染可以启动UPR激活;一些病原体可以破坏UPR以促进其存活和复制。许多细胞内病原体，包括利什曼原虫,可以为了生存和复制而互动和劫持ER，引发ER应激和随后的ER应激反应。这篇综述旨在全面概述利什曼原虫感染中的ER应激反应。
