科研队伍
胡明明

 

 最后学位:理学博士(PhD, Wuhan University)

 职称职务:教授、博导

 专业方向:细胞生物学、免疫学

 研究方向:天然免疫信号转导与代谢调控

 电话号码:027-68750121

 电子邮件:mmhu@whu.edu.cn 

 

文化经历

2007-2011 澳门百老汇生命科学学会,学士

2011-2016 澳门百老汇生命科学学会,博士

 

工作经历与任职

2016-2019 澳门百老汇4001登录网站,特聘副研究员、副教授

2019至今  澳门百老汇4001登录网站,教授、博导

 

所获荣誉与奖励

2017 澳门百老汇学术创新奖特等奖

2016 入选第一批全国优秀博士后创新人才支撑计划

 

所获研究资助

全国优秀博士后创新人才支撑计划、自然科学基金-面上项目、国家自然科学基金-优秀青年基金项目

 

代表性论文

1. Hu M.M.*, He W.R., Gao P., Yang Q., He K., Cao L.B., Li S., Feng Y.Q. and Shu H.B.* (2019). Virus-induced accumulation of intracellular bile acids activates the TGR5-b-arrestin-SRC axis to enable innate antiviral immunity. Cell Research 29, 193-205

2. Hu M.M.* and Shu H.B.* (2018). Cytoplasmic mechanisms of recognition and defense of microbial nucleic acids. Annu Rev Cell Dev Bi 34, 357-379

3. Yang, Q., Liu, T.T., Lin, H., Zhang, M., Wei, J., Luo, W.W., Hu, Y.H., Zhong, B., Hu, M.M.*, and Shu, H.B.* (2017). TRIM32-TAX1BP1-dependent selective autophagic degradation of TRIF negatively regulates TLR3/4-mediated innate immune responses. PLoS Pathog 13(9):e1006600.

4. Hu, M.M., Liao, C.Y., Yang, Q., Xie, X.Q., and Shu. H.B.* (2017). Innate immunity to RNA virus is regulated by temporal and reversible sumoylation of RIG-I and MDA5. J Exp Med 214(4):973-989.

5. Hu, M.M. and Shu H.B. (2017). Multifaceted roles of TRIM38 in innate immune and inflammatory responses. Cell Mol Immunol 14(4):331-338.

6. Hu, M.M., Yang, Q., Xie, X.Q., Liao, C.Y., Lin, H., Liu, T.T., and Shu, H.B. (2016). Sumoylation promotes the stability of the DNA sensor cGAS and the adaptor STING to regulate the kinetics of response to DNA virus. Immunity 45, 555-569.

7. Hu, M.M., Xie, X.Q., Yang, Q., Liao, C.Y., Ye, W., Lin, H., and Shu, H.B.* (2015). TRIM38 Negatively Regulates TLR3/4-Mediated Innate Immune and Inflammatory Responses by Two Sequential and Distinct Mechanisms. J Immunol 195, 4415-4425.

8. Hu, M.M., Yang, Q., Zhang, J., Liu, S.M., Zhang, Y., Lin, H., Huang, Z.F., Wang, Y.Y., Zhang, X.D., Zhong, B., and Shu, H.B. (2014). TRIM38 inhibits TNFalpha- and IL-1beta-triggered NF-kappaB activation by mediating lysosome-dependent degradation of TAB2/3. PNAS 111, 1509-1514.


 

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