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The shrimp IKK-NF-KB signaling pathway regulates antimicrobial peptide expression and may be subverted by white spot syndrome virus to facilitate viral gene expression

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Cellular & Molecular Immunology 2013年第5期10卷 423-436页

作者： pei-hui wang Zhi-Hua Gu Ding-hui Wan Bo-Du Liu Xian-De Huang Shao-Ping Weng Xiao-Qiang Yu Jian-Guo He MOE Key Laboratory of Aquatic Product Safety/State Key Laboratory of Biocontrol School of Life Sciences Sun Yat-Sen University Guangzhou China Division of Cell Biology and Biophysics School of Biological Sciences University of Missouri-Kansas City Kansas City MO USA School of Marine Sciences Sun Yat-Sen University Guangzhou China

The IκB kinases IKKα and IKKβ and the IKK-related kinases TANK-binding kinase 1 （TBK1） and IKKε are the master regulators of the NF-κB signaling pathway. Although this pathway has been extensively studied in mammals, less attention has been paid in crustaceans, which have significant economic value. Here, we report the cloning and functional studies of two IKK homologs, LvlKKβ and LvlKKε, from Pacific white shrimp, Litopenaeus vannamei. LvlKKβ and LvlKKα mRNAs are widely expressed in different tissues and are responsive to white spot syndrome virus （WSSV） infection. When overexpressed in Drosophila S2 cells, LvlKKβ but not LvlKKε activates the promoters of NF-κB pathway-controlled antimicrobial peptide genes （AMPs）, such as the Penaeidins （PENs）. In HEK 293T cells, both LvlKKβ and LvlKKε activate an NF-κB reporter. The silencing of LvlKKβ or LvlKKε using double-stranded RNA （dsRNA）-mediated RNA interference （RNAi） decreases the expression of L. vannamei AMPs, including PENs, lysozyme and crustins. Intriguingly, LvlKKβ- or LvlKKε-silenced L. vannameiare resistant to WSSV infection. We hypothesized that successful infection with WSSV requires the activation of the IKK-NF-κB signaling pathway to modulate viral gene expression. We constructed luciferase reporters for 147 WSSV genes. By screening, we found that the WSSV051, WSSV059, WSSV069, WSSV083, WSSV090, WSSV107, WSSV244, WSSV303, WSSV371 and WSSV445 promoters can be activated by LvlKKβ or LvlKKε in Drosophila S2 cells. Taken together, our results reveal that LvlKKβ and LvlKKε may participate in the regulation of shrimp AMPs and that WSSV may subvert the L. vannamei IKK-NF-κB signaling pathway to facilitate viral gene expression.

关键词： antimicrobial peptide I KK-NF-KB innate immunity Litopenaeus vannamei WSSV

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Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) membrane (M) protein inhibits type I and IIIinterferon production by targeting RIG-I/MDA-5 signaling

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Signal Transduction and Targeted Therapy 2021年第1期6卷 171-183页

作者： Yi Zheng Meng-Wei Zhuang Lulu Han Jing Zhang Mei-Ling Nan Peng Zhan Dongwei Kang Xinyong Liu Chengjiang Gao pei-hui wang Key Laboratory of Infection and Immunity of Shandong Province Department of ImmunologySchool of Basic Medical SciencesCheeloo College of MedicineShandong University250012 JinanChina Key Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute Cheeloo College of MedicineShandong University250012 JinanChina Department of Medicinal Chemistry Key Laboratory of Chemical Biology(Ministry of Education)School of Pharmaceutical SciencesCheeloo College of MedicineShandong University44 West Culture Road250012 JinanShandongPR China China–Belgium Collaborative Research Center for Innovative Antiviral Drugs of Shandong Province 44 West Culture Road250012 JinanShandongPR China Suzhou Research Institute Shandong UniversityShandong UniversitySuzhouJiangsu 215123China

Coronavirus disease 2019(COVID-19),caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has quickly spread worldwide and has affected more than 10 million individuals.A typical feature of COVID-19 is the suppression of type I and III interferon(IFN)-mediated antiviral ***,the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains ***,we reported that the SARS-CoV-2 membrane(M)protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway mediated by RIG-I/MDA-5–MAVS *** addition,the SARS-CoV-2 M protein suppresses type I and III IFN induction stimulated by SeV infection or poly(I:C)***,the SARS-CoV-2 M protein interacts with RIG-I,MAVS,and TBK1,thus preventing the formation of the multiprotein complex containing RIG-I,MAVS,TRAF3,and TBK1 and subsequently impeding the phosphorylation,nuclear translocation,and activation of ***,ectopic expression of the SARS-CoV-2 M protein facilitates the replication of vesicular stomatitis *** together,these results indicate that the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling,which subsequently attenuates antiviral immunity and enhances viral *** study provides insight into the interpretation of SARS-CoV-2-induced antiviral immune suppression and illuminates the pathogenic mechanism of COVID-19.

关键词： immunity acute MAVS

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The SARS-CoV-2 main protease induces neurotoxic TDP-43 cleavage and aggregates

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Signal Transduction and Targeted Therapy 2023年第4期8卷 1364-1367页

作者： Jiaxin Yang Yan Li Shijin wang huili Li Lili Zhang Haichen Zhang pei-hui wang Xiangyu Zheng Xiao-Fang Yu Wei Wei Institute of Virology and AIDS Research First HospitalJilin UniversityChangchunJilin 130021China Department of Neurology and Neuroscience Center First HospitalJilin UniversityChangchunJilin 130021China Key Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute Cheeloo College of MedicineShandong UniversityJinanChina Cancer Institute(Key Laboratory of Cancer Prevention and Intervention China National Ministry of Education)The Second Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiangChina Cancer Center Zhejiang UniversityHangzhouZhejiangChina Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education Institute of Translational MedicineFirst HospitalJilin UniversityChangchunJilin 130021China

Dear Editor,Neurologic manifestations associated with many COVID-19 patients,including acute infection with severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)and long COVID,have been proven by increasing evidence.1 To date,most studies have focused on how SARS-CoV-2 invades the nervous system and the consequent neuropathological changes.2,3 In contrast,the specific mechanism by which SARS-CoV-2 infection leads to neurological disease remains unclear.

关键词： acute infection respiratory

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A systemic and molecular study of subcellular localization of SARS-CoV-2 proteins

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Signal Transduction and Targeted Therapy 2020年第1期5卷 252-254页

作者： Jing Zhang Ruth Cruz-cosme Meng-Wei Zhuang Dongxiao Liu Yuan Liu Shaolei Teng pei-hui wang Qiyi Tang Advanced Medical Research Institute Cheeloo College of MedicineShandong UniversityJinanShandong 250012China Howard University College of Medicine 520 W Street NWWashingtonDC 20059USA Weill Institute for Cell and Molecular Biology Cornell UniversityIthacaNYUSA Department of Biology Howard University415 College St.NWWashingtonDC 20059USA

Dear Editor,The current pandemic of beta-coronavirus(SARS-CoV-2)has exerted devastating influence on almost all countries,resulting in the disease named COVID-19.1 Coronavirus possesses the largest RNA genome among all the RNA *** genome encodes about 29 proteins(Supplementary Fig.S1).The subcellular distributions of the viral proteins have yet been reported for *** is important to investigate the viral proteins’locations in cells because the subcellular distribution information not only helps us in understanding how viruses interact with the host cells but also provides clues in fighting against the viral ***,we cloned all the genes of SARS-CoV-2 into vectors for expression in mammalian cells and used immunofluorescent assay(IFA)to examine the viral proteins’subcellular *** for the NSP11 that is only 14 aa long,we expressed all other 28 viral proteins in HEp-2 or Caco-2 cells and found a diversity of protein distribution in cells,suggesting a complicated interaction of SARSCoV-2 with host cells to achieve a successful infection.

关键词： NSP1 fighting distribution

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Main protease of SARS-CoV-2 serves as a bifunctional molecule in restricting type I interferon antiviral signaling

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Signal Transduction and Targeted Therapy 2020年第1期5卷 646-648页

作者： Yaoxing Wu Ling Ma Zhen Zhuang Sihui Cai Zhiyao Zhao Lingli Zhou Jing Zhang pei-hui wang Jincun Zhao Jun Cui MOE Key Laboratory of Gene Function and Regulation State Key Laboratory of BiocontrolSchool of Life SciencesSun Yat-sen University510275 GuangzhouGuangdongChina State Key Laboratory of Respiratory Disease Guangzhou Institute of Respiratory DiseaseThe First Affiliated Hospital of Guangzhou Medical University510182 GuangzhouGuangdongChina Advanced Medical Research Institute Cheeloo College of MedicineShandong University250012 JinanShandongChina

Dear Editor,At present,the world is suffering from an ongoing pandemic of 2019 novel coronavirus(COVID-19)which is caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2/2019-nCoV).To date,>20 million cases were confirmed with a death toll at>700,*** there are no clinically specific and effective antiviral treatments toward SARS-CoV-2 infection so far,the pathological study of SARS-CoV-2 infection and the development of SARS-CoV-2-specific vaccines are progressing rapidly within these several months.1 However,few reports mentioned the mechanism employed by SARS-CoV-2 for evading from surveillance of immune system.

关键词： acute respiratory death

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SARS-CoV-2 NSP5 and N protein counteract the RIG-I signaling pathway by suppressing the formation of stress granules

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Signal Transduction and Targeted Therapy 2022年第2期7卷 531-542页

作者： Yi Zheng Jian Deng Lulu Han Meng-Wei Zhuang Yanwen Xu Jing Zhang Mei-Ling Nan Yang Xiao Peng Zhan Xinyong Liu Chengjiang Gao pei-hui wang Key Laboratory of Infection and Immunity of Shandong Province Department of ImmunologySchool of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China Key Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute Cheeloo College of MedicineShandong UniversityJinan 250012China Department of Medicinal Chemistry Key Laboratory of Chemical Biology(Ministry of Education)School of Pharmaceutical SciencesCheeloo College of MedicineShandong University44 West Culture Road250012 JinanShandongPR China China-Belgium Collaborative Research Center for Innovative Antiviral Drugs of Shandong Province 44 West Culture Road250012 JinanShandongPR China Suzhou Research Institute Shandong UniversityShandong UniversitySuzhouJiangsu 215123China

As a highly pathogenic human coronavirus,SARS-CoV-2 has to counteract an intricate network of antiviral host responses to establish infection and *** nucleic acid-induced stress response is an essential component of antiviral defense and is closely related to antiviral innate ***,whether SARS-CoV-2 regulates the stress response pathway to achieve immune evasion remains *** this study,SARS-CoV-2 NSP5 and N protein were found to attenuate antiviral stress granule(avSG)***,NSP5 and N suppressed IFN expression induced by infection of Sendai virus or transfection of a synthetic mimic of dsRNA,poly(I:C),inhibiting TBK1 and IRF3 phosphorylation,and restraining the nuclear translocalization of ***,HEK293T cells with ectopic expression of NSP5 or N protein were less resistant to vesicular stomatitis virus ***,NSP5 suppressed avSG formation and disrupted RIG-I–MAVS complex to attenuate the RIG-I–mediated antiviral *** contrast to the multiple targets of NSP5,the N protein specifically targeted cofactors upstream of *** N protein interacted with G3BP1 to prevent avSG formation and to keep the cofactors G3BP1 and PACT from activating ***,the N protein also affected the recognition of dsRNA by *** study revealed the intimate correlation between SARS-CoV-2,the stress response,and innate antiviral immunity,shedding light on the pathogenic mechanism of COVID-19.

关键词： NSP5 immunity stress

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城市次干路集散功能可靠度量化评价与实证研究

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交通运输系统工程与信息 2017年第2期17卷 212-218页

作者：严亚丹仝佩李辉王东炜郑州大学土木工程学院郑州450001

依据《城市道路工程设计规范》(CJJ37—2012)关于次干路功能的阐述,以"支路车流经过次干路汇集向主干路"和"主干路车流经过次干路分散到支路"为研究对象,提出城市次干路集散功能可靠度的概念,作为定量评价次干路功能实现程度的概率测度... 详细信息

依据《城市道路工程设计规范》(CJJ37—2012)关于次干路功能的阐述,以"支路车流经过次干路汇集向主干路"和"主干路车流经过次干路分散到支路"为研究对象,提出城市次干路集散功能可靠度的概念,作为定量评价次干路功能实现程度的概率测度指标,进而建立相应的数学模型.基于郑州市区2条次干路,采用实地调查的延误、信号配时和交通量数据资料,论证了非饱和情况下,车流由主干路向次干路和由次干路向支路分散,或由支路向次干路和由次干路向主路汇集的相邻交叉口左转延误的不相关性;结合模型分别计算得到各自的集功能可靠度值、散功能可靠度值,与实际交通运行状态进行对比分析,验证了所提方法的可行性与适用性.

关键词：交通工程集散功能功能可靠度次干路量化评价

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具有降糖作用的鼠李糖乳杆菌生物学特性研究

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食品工业科技 2016年第21期37卷 162-165,171页

作者：陈佩党辉王伟陈卫陕西广播电视大学陕西西安710119 陕西理工学院生物科学与工程学院陕西汉中723001 江南大学食品科学与技术国家重点实验室江苏无锡214122 陕西师范大学食品工程与营养科学学院陕西西安710119

摘要：本研究旨在评价一株具有降糖作用的鼠李糖乳杆菌的生物学特性。结果表明，该菌株生长较快，2h进入生长对数期，14h后进入稳定期，最适生长pH为5—7，最适生长温度为37℃，最适接种量为1％-2％（V／V）。此外，该菌株在强酸条件下... 详细信息

摘要：本研究旨在评价一株具有降糖作用的鼠李糖乳杆菌的生物学特性。结果表明，该菌株生长较快，2h进入生长对数期，14h后进入稳定期，最适生长pH为5—7，最适生长温度为37℃，最适接种量为1％-2％（V／V）。此外，该菌株在强酸条件下可以生长，对人工胃肠液都具有很好的耐受性，耐受胆盐的延迟时间为0．86h，在NaCI浓度为9％（W／V）的培养条件下仍可以存活。更为重要的是，这株菌对Caco-2细胞具有较强的粘附能力。综上所述：该鼠李糖乳杆菌菌株可作为一株具有潜在降糖作用的发酵菌株，用以开发具有降糖作用的新型发酵产品。

关键词：降糖鼠李糖乳杆菌生物学特性

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基于DPSIR模型的城市大气环境发展指数研究

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运筹与管理 2017年第7期26卷 147-153页

作者：杨文培何曙慧王建民杨璠中国计量大学经济与管理学院浙江杭州310018 安徽理工大学经济与管理学院安徽淮南232001 浙江经贸职业技术学院浙江杭州310018

随着我国工业化和城市化进程的不断加快,城市大气环境发展状况越来越受到学术界的关注。针对城市化进程等因素给城市大气环境带来的挑战和威胁,文章将指数的概念引入到城市大气环境评价领域,根据城市化等因素与城市大气环境发展变化之... 详细信息

随着我国工业化和城市化进程的不断加快,城市大气环境发展状况越来越受到学术界的关注。针对城市化进程等因素给城市大气环境带来的挑战和威胁,文章将指数的概念引入到城市大气环境评价领域,根据城市化等因素与城市大气环境发展变化之间的响应机理,基于DPSIR模型建立了一套城市大气环境发展指数测度指标体系与方法,并以杭州市为例,对该市2005~2014年的大气环境发展指数进行了测度和分析。文章为城市大气环境发展状况进行测度和对比分析提供了一套方法体系,使城市大气环境发展指数服务于政府管理者、城市居民等利益相关者,为城市大气环境发展管理带来新变革。

关键词：大气环境城市化环境发展指数 DPSIR

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Correction: A systemic and molecular study of subcellular localization of SARS-CoV-2 proteins

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Signal Transduction and Targeted Therapy 2021年第6期6卷 1931-1931页

作者： Jing Zhang Ruth Cruz-cosme Meng-Wei Zhuang Dongxiao Liu Yuan Liu Shaolei Teng pei-hui wang Qiyi Tang Key Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute Cheeloo College of Medicine Shandong University Jinan Shandong 250012 China Howard University College of Medicine 520 W Street NW Washington DC 20059 USA Weill Institute for Cell and Molecular Biology Cornell University Ithaca NY USA Department of Biology Howard University 415 College St. NW Washington DC 20059 USA

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