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Unfolded protein response genes regulated by CED-1 are required for Caenorhabditis elegans innate immunity.

机译:由CED-1调节的未折叠蛋白反应基因是秀丽隐杆线虫先天免疫所必需的。

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摘要

The endoplasmic reticulum stress response, also known as the unfolded protein response (UPR), has been implicated in the normal physiology of immune defense and in several disorders, including diabetes, cancer, and neurodegenerative disease. Here, we show that the apoptotic receptor CED-1 and a network of PQN/ABU proteins involved in a noncanonical UPR response are required for proper defense to pathogen infection in Caenorhabditis elegans. A full-genome microarray analysis indicates that CED-1 functions to activate the expression of pqn/abu genes. We also show that ced-1 and pqn/abu genes are required for the survival of C. elegans exposed to live Salmonella enterica, and that overexpression of pqn/abu genes confers protection against pathogen-mediated killing. The results indicate that unfolded protein response genes, regulated in a CED-1-dependent manner, are involved in the C. elegans immune response to live bacteria.
机译:内质网应激反应,也称为未折叠蛋白反应(UPR),已与免疫防御的正常生理以及包括糖尿病,癌症和神经退行性疾病在内的多种疾病有关。在这里,我们显示凋亡的受体CED-1和参与非典型UPR反应的PQN / ABU蛋白网络是对秀丽隐杆线虫病原体感染的适当防御所必需的。全基因组微阵列分析表明,CED-1的功能是激活pqn / abu基因的表达。我们还显示ced-1和pqn / abu基因对于暴露于活肠沙门氏菌的秀丽隐杆线虫的生存是必需的,并且pqn / abu基因的过表达赋予针对病原体介导的杀伤的保护。结果表明,以CED-1依赖性方式调控的未折叠蛋白应答基因参与了秀丽隐杆线虫对活细菌的免疫应答。

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