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Endoplasmic reticulum stress and fungal pathogenesis

机译:内质网应激和真菌发病机理

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摘要

The gateway to the secretory pathway is the endoplasmic reticulum (ER), an organelle that is responsible for the accurate folding, post-translational modification and final assembly of up to a third of the cellular proteome. When secretion levels are high, errors in protein biogenesis can lead to the accumulation of abnormally folded proteins, which threaten ER homeostasis. The unfolded protein response (UPR) is an adaptive signaling pathway that counters a buildup in misfolded and unfolded proteins by increasing the expression of genes that support ER protein folding capacity. Fungi, like other eukaryotic cells that are specialized for secretion, rely upon the UPR to buffer ER stress caused by fluctuations in secretory demand. However, emerging evidence is also implicating the UPR as a central regulator of fungal pathogenesis. In this review, we discuss how diverse fungal pathogens have adapted ER stress response pathways to support the expression of virulence-related traits that are necessary in the host environment
机译:分泌途径的途径是内质网(ER),它是一种细胞器,负责精确折叠,翻译后修饰和最终组装多达三分之一的细胞蛋白质组。当分泌水平高时,蛋白质生物发生中的错误会导致异常折叠的蛋白质积聚,从而威胁内质网的稳态。未折叠蛋白应答(UPR)是一种适应性信号传导途径,通过增加支持ER蛋白折叠能力的基因的表达来抵抗错误折叠和未折叠蛋白的积累。与其他专门用于分泌的真核细胞一样,真菌也依赖于UPR来缓冲由分泌需求波动引起的内质网应激。但是,新出现的证据也暗示UPR作为真菌发病机理的主要调节剂。在这篇综述中,我们讨论了各种真菌病原体如何适应内质网应激反应途径,以支持宿主环境中必需的毒力相关性状的表达。

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