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烟酰胺腺嘌呤二核苷酸磷酸氧化酶介导的氧化还原信号通过……促进抗氧化应激能力和延长寿命。 （原文in后内容缺失，翻译可能不完全准确）

NADPH oxidase-mediated redox signaling promotes oxidative stress resistance and longevity through in .

作者信息

Ewald Collin Yvès, Hourihan John M, Bland Monet S, Obieglo Carolin, Katic Iskra, Moronetti Mazzeo Lorenza E, Alcedo Joy, Blackwell T Keith, Hynes Nancy E

机构信息

Department of Health Sciences and Technology, Eidgenössische Technische Hochschule (ETH) Zürich, Zürich, Switzerland.

Friedrich Miescher Institute for Biomedical Research, University of Basel, Basel, Switzerland.

出版信息

Elife. 2017 Jan 13;6:e19493. doi: 10.7554/eLife.19493.

DOI:10.7554/eLife.19493
PMID:28085666
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5235354/
Abstract

Transient increases in mitochondrially-derived reactive oxygen species (ROS) activate an adaptive stress response to promote longevity. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases produce ROS locally in response to various stimuli, and thereby regulate many cellular processes, but their role in aging remains unexplored. Here, we identified the orthologue of mammalian mediator of ErbB2-driven cell motility, MEMO-1, as a protein that inhibits BLI-3/NADPH oxidase. MEMO-1 is complexed with RHO-1/RhoA/GTPase and loss of results in an enhanced interaction of RHO-1 with BLI-3/NADPH oxidase, thereby stimulating ROS production that signal via p38 MAP kinase to the transcription factor SKN-1/NRF1,2,3 to promote stress resistance and longevity. Either loss of or increasing BLI-3/NADPH oxidase activity by overexpression is sufficient to increase lifespan. Together, these findings demonstrate that NADPH oxidase-induced redox signaling initiates a transcriptional response that protects the cell and organism, and can promote both stress resistance and longevity.

摘要

线粒体衍生的活性氧（ROS）的短暂增加会激活适应性应激反应以促进长寿。烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶会响应各种刺激在局部产生ROS，从而调节许多细胞过程，但其在衰老中的作用仍未得到探索。在这里，我们鉴定出哺乳动物ErbB2驱动的细胞运动介导因子MEMO-1的同源物，它是一种抑制BLI-3/NADPH氧化酶的蛋白质。MEMO-1与RHO-1/RhoA/鸟苷三磷酸酶复合，其缺失会导致RHO-1与BLI-3/NADPH氧化酶的相互作用增强，从而刺激ROS产生，通过p38丝裂原活化蛋白激酶向转录因子SKN-1/NRF1、2、3发出信号，以促进应激抗性和长寿。MEMO-1的缺失或通过过表达增加BLI-3/NADPH氧化酶活性都足以延长寿命。总之，这些发现表明NADPH氧化酶诱导的氧化还原信号引发了一种保护细胞和生物体的转录反应，并可促进应激抗性和长寿。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/be91f2d26953/elife-19493-fig6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/be91f2d26953/elife-19493-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/c14aa52ff2b0/elife-19493-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/74c84679fc88/elife-19493-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/d523d72813ba/elife-19493-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/29e4574e0f9a/elife-19493-fig1-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/bdc3b4197931/elife-19493-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/698d4837b723/elife-19493-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/363eeec7963f/elife-19493-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/037b31e769e6/elife-19493-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/42f2841f7f7d/elife-19493-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/b1558dbeb261/elife-19493-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/fc0b97ad6482/elife-19493-fig5-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6e2/5235354/be91f2d26953/elife-19493-fig6.jpg

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