排序方式: 共有7条查询结果,搜索用时 156 毫秒
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Nicola Vannini Vasco Campos Mukul Girotra Vincent Trachsel Shanti Rojas-Sutterlin Josefine Tratwal Simone Ragusa Evangelos Stefanidis Dongryeol Ryu Pernille Y. Rainer Gena Nikitin Sonja Giger Terytty Y. Li Aikaterini Semilietof Aurelien Oggier Yannick Yersin Loïc Tauzin Eija Pirinen Olaia Naveiras 《Cell Stem Cell》2019,24(3):405-418.e7
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Jiebo Zhu Min Joung Lee Hee Jin Chang Xianshu Ju Jianchen Cui Yu Lim Lee Dahyun Go Woosuk Chung Eungseok Oh Jun Young Heo 《BMB reports》2022,55(4):181
Ventriculomegaly induced by the abnormal accumulation of cerebrospinal fluid (CSF) leads to hydrocephalus, which is accompanied by neuroinflammation and mitochondrial oxidative stress. The mitochondrial stress activates mitochondrial unfolded protein response (UPRmt), which is essential for mitochondrial protein homeostasis. However, the association of inflammatory response and UPRmt in the pathogenesis of hydrocephalus is still unclear. To assess their relevance in the pathogenesis of hydrocephalus, we established a kaolin-induced hydrocephalus model in 8-week-old male C57BL/6J mice and evaluated it over time. We found that kaolin-injected mice showed prominent ventricular dilation, motor behavior defects at the 3-day, followed by the activation of microglia and UPRmt in the motor cortex at the 5-day. In addition, PARP-1/NF-κB signaling and apoptotic cell death appeared at the 5-day. Taken together, our findings demonstrate that activation of microglia and UPRmt occurs after hydrocephalic ventricular expansion and behavioral abnormal-ities which could be lead to apoptotic neuronal cell death, providing a new perspective on the pathogenic mechanism of hydrocephalus. 相似文献
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S-adenosylmethionine (SAM), generated from methionine and ATP by S-adenosyl methionine synthetase (SAMS), is the universal methyl group donor required for numerous cellular methylation reactions. In Caenorhabditis elegans, silencing sams-1, the major isoform of SAMS, genetically or via dietary restriction induces a robust mitochondrial unfolded protein response (UPRmt) and lifespan extension. In this study, we found that depleting SAMS-1 markedly decreases mitochondrial SAM levels. Moreover, RNAi knockdown of SLC-25A26, a carrier protein responsible for transporting SAM from the cytoplasm into the mitochondria, significantly lowers the mitochondrial SAM levels and activates UPRmt, suggesting that the UPRmt induced by sams-1 mutations might result from disrupted mitochondrial SAM homeostasis. Through a genetic screen, we then identified a putative mitochondrial tRNA methyltransferase TRMT-10C.2 as a major downstream effector of SAMS-1 to regulate UPRmt and longevity. As disruption of mitochondrial tRNA methylation likely leads to impaired mitochondrial tRNA maturation and consequently reduced mitochondrial translation, our findings suggest that depleting mitochondrial SAM level might trigger UPRmt via attenuating protein translation in the mitochondria. Together, this study has revealed a potential mechanism by which SAMS-1 regulates UPRmt and longevity. 相似文献
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Kevin M. Tharp Ryo Higuchi-Sanabria Greg A. Timblin Breanna Ford Carlos Garzon-Coral Catherine Schneider Jonathon M. Muncie Connor Stashko Joseph R. Daniele Andrew S. Moore Phillip A. Frankino Stefan Homentcovschi Sagar S. Manoli Hao Shao Alicia L. Richards Kuei-Ho Chen Johanna ten Hoeve Gregory M. Ku Valerie M. Weaver 《Cell metabolism》2021,33(7):1322-1341.e13
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