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Ganoboninketal C from Ganoderma boninense improves the efficacy of CDDP-based chemotherapy through inhibiting translesion DNA synthesis

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Food Science and Human Wellness 2024年第5期13卷 2982-2992页

作者： Xiaolu Ma Fei Yang Ke Ma Hongyan Shen Junjie Han Kai Wang Yeran Yang Jiawei Zhu Ruiyuan An Qilin Wang tie-shan tang Bo Zhou Hongwei Liu Caixia Guo College of Biomedical Engineering Taiyuan University of TechnologyTaiyuan 030024China CAS Key Laboratory of Genomics and Precision Medicine Beijing Institute of Genomics/China National Center for BioinformationUniversity of Chinese Academy of SciencesChinese Academy of SciencesBeijing 100101China State Key Laboratory of Membrane Biology Institute of ZoologyUniversity of Chinese Academy of SciencesChinese Academy of SciencesBeijing 100101China Institute of Microbiology University of Chinese Academy of SciencesChinese Academy of SciencesBeijing 100101China Beijing Institute for Stem Cell and Regenerative Medicine Beijing 100101China University of Chinese Academy of Sciences Chinese Academy of SciencesBeijing 100101China

Translesion DNA synthesis(TLS)can bypass DNA lesions caused by chemotherapeutic drugs,which usually result in drug *** its key role in mutagenesis and cell survival after DNA damage,inhibition of the TLS pathway has emerged as a potential target for improving the efficacy of DNA-damaging agents such as cisplatin(CDDP),a widely used anticancer ***,few suitable natural TLS inhibitors have been ***,we found that a triterpenoid compound Ganoboninketal C(26-3)from Ganoderma boninense,a traditional Chinese medicine,can impair CDDP-induced TLS polymerase eta(Polη)focus formation,PCNA monoubiquitination as well as ***,26-3 can significantly sensitize tumor cells to CDDP killing and reduce the proportion of cancer stem cells in AGS and promote apoptosis after CDDP ***,26-3 can also sensitize tumor cells to Gefitinib ***,through RNA-seq analysis,we found that 26-3 could abrogate the CDDP-induced upregulation of Polηand PIDD(p53-induced protein with a death domain),2 known factors promoting TLS ***,we found that activating transcription factor 3 is a potential novel TLS *** together,we have identified a natural TLS inhibitor 26-3,which can be potentially used as an adjuvant to improve clinical efficacy.

关键词： Ganoderma boninense Ganoboninketal C Cisplatin chemotherapy Translesion DNA synthesis

Miro2 supplies a platform for Parkin translocation to damaged mitochondria

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Science Bulletin 2019年第11期64卷 730-747页

作者： Jiu-Qiang Wang Shu Zhu Yihan Wang Fengli Wang Chaoqiang An Dongfang Jiang Lijie Gao Yingfeng Tu Xuefei Zhu Yun Wang Hongmei Liu Juanjuan Gong Zhongshuai Sun Xi Wang Leimei Liu Keyan Yang Caixia Guo tie-shan tang State Key Laboratory of Membrane Biology Institute of ZoologyUniversity of Chinese Academy of SciencesChinese Academy of SciencesBeijing 100101China Key Laboratory of Genomics and Precision Medicine Beijing Institute of GenomicsUniversity of Chinese Academy of SciencesChinese Academy of SciencesBeijing 100101China Department of Foresight and Evaluation Research Chinese Academy of Science and Technology for DevelopmentBeijing 100038China Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijing 100101China

PINK1/Parkin-mediated mitophagy is an important process in selective removal of damaged mitochondria, in which translocation of Parkin to damaged mitochondria is recognized as an initiation step. At present, how the damaged mitochondria are selectively recognized and targeted by Parkin is not fully understood. Here we show that Miro2, an outer mitochondrial membrane protein, undergoes demultimerization from a tetramer to a monomer and alteration in mitochondrial localization upon CCCP treatment, suggesting a CCCP-induced realignment of Miro2. The realignment of Miro2 is tightly regulated by PINK1-mediated phosphorylation at Ser325/Ser430 and by Ca^2+binding to EF2 domain, which are both essential for the subsequent Parkin translocation. Interestingly, ablation of Miro2 in mouse causes delayed reticulocyte maturation, lactic acidosis and cardiac disorders. Furthermore, several Miro2 mutations found in the congenital lactic acidosis patients also disable its realignment and Parkin translocation. These findings reveal an important role of Miro2 to mediate Parkin translocation by sensing both depolarization and Ca^2+release from damaged mitochondria to ensure the accuracy of mitophagy.

关键词： Miro2 Parkin Mitochondria Ca^2+ Mitophagy PINK1

Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction

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Protein & Cell 2020年第1期11卷 1-22页

作者： Si Wang Zheying Min Qianzhao Ji Lingling Geng Yao Su Zunpeng Liu Huifang Hu Lixia Wang Weiqi Zhang Keiichiro Suzuiki Yu Huang Puyao Zhang tie-shan tang Jing Qu Yang Yu Guang-Hui Liu Jie Qiao Department of Obstetrics and Gynecology Center for Reproductive MedicinePeking University Third HospitalBeijing 100191China National Laboratory of Biomacromolecules CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China Institute for Stem cell and Regeneration Chinese Academy of SciencesBeijing 100101China Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China Beijing Institute for Brain Disorders Beijing 100069China Institute for Advanced Co-Creation Studies Osaka UniversityOsaka 560-8531Japan Graduate School of Engineering Science Osaka UniversityOsaka 560-8531Japan Department of Medical Genetics School of Basic Medical SciencesPeking University Health Science CenterBeijing 100191China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Peking-Tsinghua Center for Life Sciences Academy for Advanced Interdisciplinary StudiesPeking UniversityBeijing 100871China

Cockayne syndrome(CS)is a rare autosomal recessive inherited disorder characterized by a variety of clinical features,including increased sensitivity to sunlight,progressive neurological abnormalities,and the appearance of premature ***,the pathogenesis of CS remains unclear due to the limitations of current disease ***,we generate integration-free induced pluripotent stem cells(iPSCs)from fibroblasts from a CS patient bearing mutations in CSB/ERCC6 gene and further derive isogenic genecorrected CS-iPSCs(GC-iPSCs)using the CRISPR/Cas9 ***-associated phenotypic defects are recapitulated in CS-iPSC-derived mesenchymal stem cells(MSCs)and neural stem cells(NSCs),both of which display increased susceptibility to DNA damage *** aging defects in CS-MSCs are rescued by the targeted correction of mutant *** next map the transcriptomic landscapes in CS-iPSCs and GC-iPSCs and their somatic stem cell derivatives(MSCs and NSCs)in the absence or presence of ultraviolet(UV)and replicative stresses,revealing that defects in DNA repair account for CS ***,we generate autologous GC-MSCs free of pathogenic mutation under a cGMP(Current Good Manufacturing Practice)-compliant condition,which hold potential for use as improved biomaterials for future stem cell replacement therapy for ***,our models demonstrate novel disease features and molecular mechanisms and lay a foundation for the development of novel therapeutic strategies to treat CS.

关键词： Cockayne syndrome CRISPR/Cas9 gene correction disease modelling mesenchymal stem cell neural stem cell

Correction to:Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction

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Protein & Cell 2022年第8期13卷 623-625页

作者： Si Wang Zheying Min Qianzhao Ji Lingling Geng Yao Su Zunpeng Liu Huifang Hu Lixia Wang Weiqi Zhang Keiichiro Suzuiki Yu Huang Puyao Zhang tie-shan tang Jing Qu Yang Yu Guang-Hui Liu Jie Qiao Department of Obstetrics and Gynecology Center for Reproductive MedicinePeking University Third HospitalBeiing 100191China National Laboratory of Biomacromolecules CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBejing 100101China University of Chinese Academy of Sciences Bejjing 100049China Advanced Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China Institute for Stem cell and Regeneration Chinese Academy of SciencesBeijing 100101China Key Laboratory of Genomic and Precision Medicine Beiing Institute of GenomicsChinese Academy of SciencesBeijing 100101China Beijing Institute for Brain Disorders Beijing 100069China Institute for Advanced Co-Creation Studies Osaka UniversityOsaka 560-8531Japan Graduate School of Engineering Science Osaka UniversityOsaka 560-8531Japan Department of Medical Genetics School of Basic Medical SciencesPeking University Health Science CenterBeijing 100191China State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeiing 100101China Peking-Tsinghua Center for Life Sciences Academy forAdvancedInterdisciplinary StudiesPeking UniversityBeijing 100871China

CORRECTION TO:PROTEIN CELL HTTPS://***/10.1007/S13238-019-0623-2 In Fig.7C,we used the ***(CS iPSCs)as NANOG positive control pluripotent cells in the upper ***,these cells were inadvertently labeled as ERCC6^(GC)-*** the revised version of Fig.7C,we have updated the high-quality images along with the corrected *** addition,we have also made corresponding chan-ges in the figure legend.

关键词： CRISPR/Cas9 Rescue correction

Dysregulation of mitochondrial calcium signaling and superoxide flashes cause mitochondrial genomic DNA damage in Huntington's disease

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Dysregulation of mitochondrial calcium signaling and superox...

Genome-wide loss of 5-hmC is a novel epigenetic feature of huntington's disease

中国神经科学学会第十届全国学术会议

作者： Jiu-Qiang WANG Qian CHEN Xian-Hua WANG Qiao-Chu WANG Yun WANG He-Ping CHENG Cai-Xia GUO Qin-Miao SUN Quan CHEN tie-shan tang State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of ZoologyChinese Academy of Sciences State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Molecular MedicinePeking University Laboratory of Disease Genomics and Individual Medicine Beijing Institute of GenomicsChinese Academy of Sciences

Objective Huntington’s disease(HD) is an inherited,fatal neurodegenerative disorder characterized by the progressive loss of striatal medium spiny *** previous research found that cytoplasmic Ca was disordered due to mutant Huntington abnormally binding to ***,Indications of oxidative stress are apparent in brain tissues from both HD patients and HD mouse models;however,the origin of this oxidant stress remains a *** present study used a yeast artificial chromosome transgenic mouse model of HD(YAC128) to explore the potential connections between dysregulation of cytosolic Ca signaling and mitochondrial oxidative damage in HD *** Changes of mitochondrial Ca and superoxide flashes were measured with TIRF fluorescence *** efficiency of knocking-down was determined with western ***(1) YAC128 embryonic fibroblasts(MEFs)exhibit a strikingly higher level of mitochondrial matrix Ca loading and elevated superoxide generation compared to WT cells.(2) The excessive mitochondrial oxidant stress is critically dependent on mitochondrial Ca loading in HD cells,since blocking mitochondrial Ca uptake abolished elevated superoxide generation.(3) Similar results were obtained in neurons from HD model mice and fibroblast cells from HD patient.(4) Mitochondrial Ca loading in HD cells caused a 2-fold higher level of mitochondrial genomic DNA(mtDNA) damage due to the excessive oxidant generation.

关键词： huntington’s disease mitochondria superoxide flashes Ca2+

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Genome-wide loss of 5-hmC is a novel epigenetic feature of h...

TMCO1 functions as an ER Ca2+ load-activated Ca2+(CLAC) release channel

中国神经科学学会第十届全国学术会议

作者： Feng-Li WANG Ye-Ran YANG Xi-Wen LIN Jiu-Qiang WANG Yong-Sheng WU Wen-Juan XIE Dan-Dan WANG Shu Zhu You-Qi LIAO Qin-Miao SUN Yun-Gui YANG Cai-Xia GUO Chun-Sheng HAN tie-shan tang The State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of ZoologyChinese Academy of Sciences Laboratory of Disease Genomics and Individual Medicine Beijing Institute of GenomicsChinese Academy of Sciences State Key Laboratory of Reproductive Biology Institute of ZoologyChinese Academy of Sciences

Objective 5-hydroxymethylcytosine(5-hmC) may represent a new epigenetic modification of *** the dynamics of 5-hmC during neurodevelopment have recently been reported,little is known about its genomic distribution and function(s) in neurodegenerative diseases such as Huntington’s disease(HD).Methods To gain a genome-wide view of 5-hmC distribution,we employed a 5-hmC-specific chemical labeling and enrichment technology coupled with high-throughput deep sequencing of 5-hmC-containing DNA *** and cortical DNA samples from the brains of 3-month-old WT7YAC128 mice were prepared and deeply sequenced to determine the effect of HTT on the 5-hmC epigenome at the early stage of *** We observed a marked reduction of 5-hmC signal in YAC128 HD mouse brain *** genomic features of 5-hmC are highly conserved,not being affected by either disease or brain *** have identified disease-specific(YAC128 versus WT) differentially hydroxymethylated regions(DhMRs),and found that acquisition of DhmRs in gene body is a positive epigenetic regulator for gene *** pathway analysis of genotype-specific DhMR-annotated genes revealed that alternation of a number of canonical pathways involving neuronal development/differentiation(Wnt/β-catenin/Sox pathway,axonal guidance signaling pathway) and neuronal function/survival(glutamate receptor/calcium/CREB,GABA receptor signaling,dopamine-DARPP32 feedback pathway etc.) could be important for the onset of *** Genome-wide Loss of 5-hmC is a Novel Epigenetic Feature of Huntington’s Disease and the first genome-wide maps of 5-hmC in striatum and cortex from both WT and YAC128 HD mice brains were generated.

关键词： 5-hydroxymethylcytosine Huntington’s disease differentially hydroxymethylated regions(DhMRs) pathway analysis

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TMCO1 functions as an ER Ca2+ load-activated Ca2+(CLAC) rele...

Multi-Innovation Gradient Iterative Locally Weighted Learning Identification for A Nonlinear Ship Maneuvering System

第十一届全国钙信号和细胞功能研讨会

作者： Qiao-Chu Wang Qiaoxia Zheng Haiyan Tan Bing Zhang Xiaoling Li Yuxiu Yang Jie Yu Yang Liu Hao Chai Xi Wang Zhongshuai Sun Jiu-Qiang Wang Shu Zhu Fengli Wang Maojun Yang Caixia Guo Heng Wang Qingyin Zheng Yang Li Quan Chen Aimin Zhou tie-shan tang State Key Laboratory of Membrane Biology Institute of Zoology Chinese Academy of Sciences Department of Chemistry and GRHD Cleveland State University CAS key Laboratory of Receptor Research Shanghai Institute of Materia Medica Chinese Academy of Sciences Key Laboratory for Protein Sciences of Ministry of Education Tsinghua-Peking Center for Life Sciences School of Life Sciences Tsinghua University Key Laboratory of Genomics and Precision Medicine China Gastrointestinal Cancer Research Center Beijing Institute of Genomics Chinese Academy of Sciences

Endoplasmic reticulum(ER) Ca store homeostasis is crucial for the proper Ca signaling and cellular functions. It has been established that Ca-release-activated Ca(CRAC) channel is responsible for the Ca influx and Ca store refilling after store depletion. However, it is unclear whether the ER Ca store can expel the excess Ca when the store gets overloaded. Here we show that TMCO1 is an ER transmembrane protein that actively prevents Ca store from overfilling. TMCO1 undergoes reversible homo-tetramerization/disassembly in response to ER Ca overloading/depletion, and forms a Ca selective ion channel on giant-liposomes. TMCO1-knockout mice reproduce the main clinical features of human cerebrofaciothoracic(CFT) dysplasia spectrum and exhibit a severe mishandling of ER Ca in cells. These findings reveal TMCO1 to be a novel Ca channel for ER Ca homeostatic maintenance. We name this Ca load-activated Ca channel "CLAC" channel, a function disrupted by human CFT dysplasia spectrum mutations.

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China Ocean Engineering 2018年第3期32卷 288-300页

作者： BAI Wei-wei REN Jun-sheng LI tie-shan Navigation College Dalian Maritime University

This paper explores a highly accurate identification modeling approach for the ship maneuvering motion with fullscale trial. A multi-innovation gradient iterative(MIGI) approach is proposed to optimize the distance metric of locally weighted learning(LWL), and a novel non-parametric modeling technique is developed for a nonlinear ship maneuvering system. This proposed method’s advantages are as follows: first, it can avoid the unmodeled dynamics and multicollinearity inherent to the conventional parametric model; second, it eliminates the over-learning or underlearning and obtains the optimal distance metric; and third, the MIGI is not sensitive to the initial parameter value and requires less time during the training phase. These advantages result in a highly accurate mathematical modeling technique that can be conveniently implemented in applications. To verify the characteristics of this mathematical model, two examples are used as the model platforms to study the ship maneuvering.

关键词： multi-innovation gradient iterative(MIGI) locally weighted learning(LWL) identification nonlinearship maneuvering full-scale trial

Engineering morphologies of cobalt oxide/phosphate-carbon nanohybrids for high-efficiency electrochemical water oxidation and reduction

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Journal of Energy Chemistry 2021年第1期30卷 139-146,I0005页

作者： shan-shan Xu Xian-Wei Lv Yan-Mei Zhao tie-Zhen Ren Zhong-Yong Yuan Hebei Provincial Key Laboratory of Green Chemical Technology&High Efficient Energy Saving School of Chemical Engineering and TechnologyHebei University of TechnologyTianjin 300130China Key Laboratory of Advanced Energy Materials Chemistry(Ministry of Education) School of Materials Science and EngineeringNankai UniversityTianjin 300350China State Key Laboratory of High-efficiency Utilization of Coal and Green Chemical Engineering Ningxia UniversityYinchuan 750021NingxiaChina

Active non-noble metal catalysts plays a decisive role for water electrolysis,however,the rational design and development of cost-efficient electrocatalysts with Pt/IrO2-like activity is still a challenging ***,a facile one-step electrodeposition route in deep eutectic solvents(DESs) is developed for morphology-controllable synthesis of cobalt oxide/phosphate-carbon nano hybrids on nickel foam(CoPO@C/NF).A series of CoPO@C/NF nanostructures including cubes,octahedrons,microspheres and nanoflowers are synthesized,which show promising electrocatalytic properties toward oxygen and hydrogen evolution reactions(OER/HER).Such surface self-organized microstructure with accessible active sites make a significant contribution to the enhanced electrochemical activity,and hybridizing cobalt oxide with cobalt pyrophosphates and carbon can result in enhanced OER performance through synergistic *** all nanostructures,the obtained microspherical CoPO@C/NF-3 catalyst exhibits excellent catalytic activities for OER and HER in 1.0 M KOH,affording an anodic current density of 10 mA cm^(-2) at overpotentials of 293 mV for OER and 93 mV for HER,with good long-time *** work offers a practical route for engineering the high-performance electrocatalysts towards efficient energy conversion and storage devices.

关键词： Cobalt-based electrocatalysts Oxygen evolution reaction Hydrogen evolution reaction Deep eutectic solvents Electrodeposition