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| 1 | C.elegans-based screen identifies lysosome-damaging alkaloids that induce STAT3-dependent lysosomal cell death显示文摘Lysosomes are degradation and signaling centers within the cell,and their dysfunction impairs a wide variety of cellular processes.To understand the cellular effect of lysosome damage,we screened natural smallmolecule compounds that induce iysosomal abnormality using Caenorhabditis elegans (C.elegans)as a model system.A group of vobasinyl-ibogan type bisindole alkaloids (ervachinines A-D)were identified that caused lysosome enlargement in C.elegans macrophage-like cells.Intriguingly,these compounds triggered cell death in the germ line independently of the canonical apoptosis pathway.In mammalian cells, ervachinines A-D induced lysosomal enlargement and damage,leading to leakage of cathepsin proteases, inhibition of autophagosome degradation and necrotic cell death.Further analysis revealed that this ervachinine-induced lysosome damage and lysosomal cell death depended on STAT3 signaling,but not RIP1 or RIP3 signaling.These findings suggest that lysosomedamaging compounds are promising reagents for dissecting signaling mechanisms underlying lysosome homeostasis and lysosome-related human disorders. | Yang Li Yu Zhang Qiwen Gan Meng Xu Xiao Ding Guihua Tang Jingjing Liang Kai Liu Xuezhao Liu Xin Wang Lingli Guo Zhiyang Gao Xiaojiang Hao Chonglin Yang | 2018 | Protein & Cell2018，9，12： | 2 |
| 2 | Defective arginine metabolism impairs mitochondrial homeostasis in Caenorhabditis elegans显示文摘Arginine catabolism involves enzyme-dependent reactions in both mitochondria and the cytosol,defects in which may lead to hyperargininemia,a devastating developmental disorder.It is largely unknown if defective arginine catabolism has any effects on mitochondria.Here we report that normal arginine catabolism is essential for mitochondrial homeostasis in Caenorhabditis elegans.Mutations of the arginase gene argn-1 lead to abnormal mitochondrial enlargement and reduced adenosine triphosphate(ATP)production in C elegans hypodermal cells.ARGN-1 localizes to mitochondria and its loss causes arginine accumulation,which disrupts mitochondrial dynamics.Heterologous expression of human ARGl or ARG2 rescued the mitochondrial defects of argn-1 mutants.Importantly,genetic inactivation of the mitochondrial basic amino acid transporter SLC-25A29 or the mitochondrial glutamate transporter SLC-25A18.1 fully suppressed the mitochondrial defects caused by argn-1 mutations.These findings suggest that mitochondrial damage probably contributes to the pathogenesis of hyperargininemia and provide clues for developing therapeutic treatments for hyperargininemia. | Ruofeng Tang Xin Wang Junxiang Zhou Fengxia Zhang Shan Zhao Qiwen Gan Liyuan Zhao Fengyang Wang Qian Zhang Jie Zhang Guodong Wang Chonglin Yang | 2020 | Journal of Genetics and Genomics2020，47，3： | 2 |
| 3 | Lentivirus-mediated gene silencing of KLF8 reduced the proliferation and invasion of gastric cancer cells显示文摘 | Gang Chen Wenjun Yang Weidong Jin Yi Wang Chonglin Tao Zhengping Yu | 2012 | Molecular Biology Reports2012，，10： | 1 |
| 4 | An everlasting role of animal models in understanding human disease显示文摘Model organisms have been widely used to dissect important biological phenomena, as well as to explore potential causes and treatments for human disorders. Much of our knowledge on molecular mechanisms underlying the heredity, development as well as physiology is largely derived from the researches of model organisms. We have | Dr. Xiao Yang Genetic Laboratory of Development and Diseases, State Key Laboratory of Proteomics, Institute of Biotechnology, Beijing 100071, China Dr. Chonglin Yang Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100190, China | 2010 | Journal of Genetics and Genomics2010，37，9： | 1 |
| 5 | Rapid and durable oxygen reduction reaction enabled by a perovskite oxide with self-cleaning surface显示文摘The growth of electrochemically inert segregation layers on the surface of solid oxide fuel cell cathodes has become a bottleneck restricting the development of perovskite-structured oxygen reduction catalysts.Here,we report a new discovery in which enriched Ba and Fe ions on the near-surface of Nd_(1/2)Ba_(1/2)Co_(1/3)Fe_(1/3)Mn_(1/3)O_(3-δ)spontaneously agglomerate into dispersed Ba_(5)Fe_(2)O_(8) nanoparticles and maintain a highly active and durable perovskite structure on the surface.This unique surface selfcleaning phenomenon is related to the low average potential energy of Ba_(5)Fe_(2)O_(8),which is grown on the near-surface layer.The electrochemically inert Ba_(5)Fe_(2)O_(8) segregation layer on the near-surface of the perovskite catalyst achieves self-cleaning by regulating the formation energy of enriched metal oxides.This self-cleaned perovskite surface exhibits an ultrafast oxygen exchange rate,high catalytic activity for the oxygen reduction reaction,and good adaptability to the actual working conditions of solid oxide fuel cell stacks.This study paves a new way for overcoming the stubborn problem of perovskite catalyst surface deactivation and enriches the scientific knowledge of surface catalysis. | Shengli Pang Yifan Song Meng Cui Xin Tang Chao Long Lingfeng Ke Gongmei Yang Ting Fang Yong Guan Chonglin Chen | 2023 | Journal of Energy Chemistry2023，，8： | 0 |
| 6 | Signal waveform design to detect an underwater high-speed small target显示文摘The problem of sonar signal waveform design to detect a high-speed small target in an underwater environment is discussed. From theoretical analysis, time-frequency hop signal is regarded as the most suitable signal waveform in this application. To get precise target parameter estimation ability, the signal should have high range-Doppler resolution performance. The results of signal analysis show that hop signal with frequency serial coding as Costas array has sharp ambiguity characteristic, so it can be used in an active sonar system to detect a high speed small target. A scheme of frequency coding is also presented. | YANG Chonglin YAO Lan (Shanghai marine electronic equipment research institute Shanghai 200025) | 2002 | Chinese Journal of Acoustics2002，21，1： | 0 |
| 7 | MRG-1 is required for genomic integrity in Caenorhabditis elegans germ cells显示文摘在 meiotic 房间分割期间,合适的染色体联会和 DNA 双海滨裂缝(DSB ) 的精确修理被要求维持 genomic 完整,哪个导致 apoptosis 的损失或 meiotic 缺点。位于 meiotic 染色体联会, DSB 修理和 apoptosis 下面的机制充分没被理解。这里,我们报导包含 chromodomain 蛋白质 MRG-1 是为在在 Caenorhabditis elegans 的成熟分裂的 genomic 完整的一个重要因素。mrg-1 功能的损失导致了被影响 DNA 损坏检查点基因的变化部分禁止的细菌房间 apoptosis 的重要增加。一致地, mrg-1 异种细菌线展出了 SPO-11-generated DSB 并且提高了外长的 DNA 在 diakinesis 的导致损坏的染色体破碎。另外,在 mrg-1 异种的过多的 apoptosis 被联会检查点基因 pch-2 的损失部分压制,并且 meiotic 原子核的一个重要数字在染色质上与 H3K9me2 的提高的水平在 leptotene/zygotene 阶段积累了,它同样在在 synaptonemal 建筑群缺乏的异种被观察,建议染色体联会的合适的前进多半当 mrg-1 不在时被损害。总的来说,这些调查结果建议 MRG-1 为由在成熟分裂支持 meiotic DSB 修理和联会前进的 genomic 正直是批评的。 | Jing Xu Xiaojuan Sun Yudong Jing Mo Wang Kai Liu Youli Jian Mei Yang Zhukuan Cheng Chonglin Yang | 2012 | Cell Research2012，22，5： | 0 |
| 8 | A pair of transporters controls mitochondrial Zn^(2+) levels to maintain mitochondrial homeostasis显示文摘Zn^(2+)is required for the activity of many mitochondrial proteins,which regulate mitochondrial dynamics,apoptosis and mitophagy.However,it is not understood how the proper mitochondrial Zn^(2+)level is achieved to maintain mitochondrial homeostasis.Using Caenorhabditis elegans,we reveal here that a pair of mitochondrion-localized transporters controls the mitochondrial level of Zn^(2+).We demonstrate that SLC-30A9/ZnT9 is a mitochondrial Zn^(2+)exporter.Loss of SLC-30A9 leads to mitochondrial Zn^(2+)accumulation,which damages mitochondria,impairs animal development and shortens the life span.We further identify SLC-25A25/SCaMC-2 as an important regulator of mitochondrial Zn^(2+)import.Loss of SLC-25A25 suppresses the abnormal mitochondrial Zn^(2+)accumulation and defective mitochondrial structure and functions caused by loss of SLC-30A9.Moreover,we reveal that the endoplasmic reticulum contains the Zn^(2+)pool from which mitochondrial Zn^(2+)is imported.These findings establish the molecular basis for controlling the correct mitochondrial levels for normal mitochondrial structure and functions. | Tengfei Ma Liyuan Zhao Jie Zhang Ruofeng Tang Xin Wang Nan Liu Qian Zhang Fengyang Wang Meijiao Li Qian Shan Yang Yang Qiuyuan Yin Limei Yang Qiwen Gan Chonglin Yang | 2022 | Protein & Cell2022，13，3： | 0 |
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