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个人简介

教育及工作经历: 1992-1996:华中农业大学,土壤与植物营养专业,学士 1996-2002:华中农业大学,微生物学专业,博士 2002-2005:法国里昂第一大学感染与免疫学系,博士后 2005-2009:美国克利夫兰临床医院,分子遗传学系,博士后 2009-至今:武汉大学生命科学学院,病毒学国家重点实验室,教授

研究领域

1)系统阐明了病毒聚合酶和核心蛋白相互作用能够形成一种特殊的结构-包涵体,它担负病毒RNA合成的新功能;2)深入研究了病毒基质蛋白调节病毒粒子组装和释放的新机制;3)发现病毒基质蛋白和聚合酶协同调节/劫持细胞自噬过程,从而最大限度增强病毒的复制和感染能力;4)解析了病毒逃逸宿主细胞应激颗粒抗病毒反应的分子机制,提出弱化病毒复制和感染的新策略。

近期论文

查看导师新发文章 (温馨提示:请注意重名现象,建议点开原文通过作者单位确认)

1. Yang X, Hu Z, Zhang Q, Fan S, Zhong Y, Guo D, Qin Y, Chen M*. 2019. SG formation relies on eIF4GI-G3BP interaction which is targeted by picornavirus stress antagonists. Cell Discov. eCollection. 2. Zhang L, Qin Y, Chen M*. Viral strategies for triggering and manipulating mitophagy. Autophagy. 2018. 14(10):1665-1673. 3. Zhang S#, Cheng Q#, Luo C, Qin Y*, Chen M*. Human Parainfluenza Virus Type 3 Matrix Protein Reduces Viral RNA Synthesis of HPIV3 by Regulating Inclusion Body Formation. Viruses. 2018. 11;10(3). 4. Hu Z, Wang Y, Tang Q, Yang X, Qin Y, Chen M*. Inclusion bodies of human parainfluenza virus type 3 inhibit antiviral stress granule formation by shielding viral RNAs. PLoS Pathog. 2018. 14(3): e1006948. 5. Yang X, Hu Z, Fan S, Zhang Q, Zhong Y, Guo D, Qin Y, Chen M*. Picornavirus 2A protease regulates stress granule formation to facilitate viral translation. PLoS Pathog. 2018. 14(2): e1006901. 6. Zhang S#, Cheng Q#, Luo C, Yin L, Qin Y*, Chen M*. An alanine residue in human parainfluenza virus type 3 phosphoprotein is critical for restricting excessive N0-P interaction and maintaining N solubility. Virology. 2018. 518:64-76. 7. Ding B#, Zhang L#, Li Z, Zhong Y, Tang Q, Qin Y, Chen M*. The Matrix Protein of Human Parainfluenza Virus Type 3 Induces Mitophagy that Suppresses Interferon Responses. Cell Host & Microbe. 2017. 21(4):538-547. 8. Zhang S#, Jiang Y#, Cheng Q, Zhong Y, Qin Y, Chen M*. Inclusion body fusion of human parainfluenza virus type 3 regulated by acetylated α-tubulin enhances viral replication. Journal of Virology. 2017. 91(3). pii: e01802-16. 9. Jiang Y, Qin Y*, Chen M*. Host-Pathogen Interactions in Measles Virus Replication and Anti-Viral Immunity. Viruses. 2016. 8 (11), E308 (Invited review). 10. Yan Q#, Wu L#, Chen L, Qin Y*, Pan Z*, Chen M*. Vesicular stomatitis virus-based vaccines expressing EV71 virus-like particles elicit strong immune responses and protect newborn mice from lethal challenges. Vaccine. 2016. 34:4196-4204. 11. Zhang G#, Zhong Y#, Qin Y, Chen M*. Interaction of Human Parainfluenza Virus Type 3 Nucleoprotein with Matrix Protein Mediates Internal Viral Protein Assembly. Journal of Virology. 2015. 90(5):2306-15. 12. Ding B, Qin Y, Chen M*. Nucleocapsid proteins: roles beyond viral RNA packaging. WIREs RNA. 2016. 7(2):213-26. (Invited review). 13. Chen L, Zhong Y, Hu Z, Qin Y. Chen M. Chen M*. Two second-site mutations compensate the engineered mutation of R7A in vesicular stomatitis virus nucleocapsid protein. Virus Research. 2016. 214:59-64. 14. Chen L#, Yan Q#, Lu G, Hu Z, Zhang G, Zhang S, Ding B, Jiang Y, Zhong Y, Gong P, Chen M*. Several residues within the N-terminal arm of vesicular stomatitis virus nucleoprotein play a critical role in protecting viral RNA from nuclease digestion. Virology. 2015. 478:9-17. 15. Ding B, Zhang G, Yang X, Zhang S, Chen L, Yan Q, Xu M, Banerjee AK, Chen M*. Phosphoprotein of human parainfluenza virus type 3 blocks autophagosome-lysosome fusion to increase virus production. Cell Host & Microbe. 2014. 15(5):564-77. 16. Zhang G, Zhang S, Ding B, Yang X, Chen L, Yan Q, Jiang Y, Zhong Y, Chen M*. A Leucine Residue in C-terminus of Human Parainfluenza Virus Type 3 Matrix Protein Is Essential for Efficient Virus-Like Particle and Virion Release. Journal of Virology. 2014. 88(22):13173-88. 17. Zhang S, Chen L, Zhang G, Yan Q, Yang X, Ding B, Tang Q, Sun S, Hu Z, Chen M*. An amino acid of human parainfluenza virus type 3 nucleoprotein is critical for template function and cytoplasmic inclusion body formation. Journal of Virology. 2013. 87(22):12457-70. 18. Chen L, Zhang S, Banerjee AK and Chen M*. N-Terminal Phosphorylation of Phosphoprotein of Vesicular Stomatitis Virus Is Required for Preventing Nucleoprotein from Binding to Cellular RNAs and for Functional Template Formation. Journal of Virology. 2013. 87(6):3177-86.

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