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As a toxin dies a prion comes to life: A tentative natural history of the [Het-s] prion

机译:由于毒素死亡,朊病毒来到生命:[het-s]朊病毒的暂定自然历史

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摘要

A variety of signaling pathways, in particular with roles in cell fate and host defense, operate by a prion-like mechanism consisting in the formation of open-ended oligomeric signaling complexes termed signalosomes. This mechanism emerges as a novel paradigm in signal transduction. Among the proteins forming such signaling complexes are the Nod-like receptors (NLR), involved in innate immunity. It now appears that the [Het-s] fungal prion derives from such a cell-fate defining signaling system controlled by a fungal NLR. What was once considered as an isolated oddity turns out to be related to a conserved and widespread signaling mechanism. Herein, we recall the relation of the [Het-s] prion to the signal transduction pathway controlled by the NWD2 Nod-like receptor, leading to activation of the HET-S pore-forming cell death execution protein. We explicit an evolutionary scenario in which formation of the [Het-s] prion is the result of an exaptation process or how a loss-of-function mutation in a pore-forming cell death execution protein (HET-S) has given birth to a functional prion ([Het-s]).
机译:特别是在细胞命运和宿主防御中具有统一的各种信号通路,通过朊病毒机构操作,该机构包括形成的开口未结束的低聚信号传递复合物称为信号弹素。这种机制出现为信号转导的新型范式。形成这种信号配合物的蛋白质是涉及先天免疫的NOD样受体(NLR)。现在似乎[HET-S]真菌朊病毒源于定义由真菌NLR控制的信号系统的这种细胞命运。一旦被认为是孤立的奇怪,曾经被认为是与保守和广泛的信号传导机制相关的。在此,我们回顾[HET-S]朊病毒对由NWD2 NOD样受体控制的信号转导途径的关系,导致HET-S孔形成细胞死亡执行蛋白的激活。我们明确了一种进化场景,其中[HET-S]朊病毒是展开过程的结果或孔形成细胞死亡执行蛋白(HET-S)中的功能突变如何生育功能朊病毒([het-s])。

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