担任 | 复旦大学上海医学院免疫学系副教授 |
学习与科研 | 2001.09-2004.07 南昌大学医学院病原生物学系硕士研究生 2004.07-2005.07 深圳大学生命科学学院，微生物基因工程重点实验室 助教 2005.09-2008.06 复旦大学上海医学院免疫学系 博士研究生 2008.07-2011.03 复旦大学上海医学院免疫学系 讲师 2011.04-至今 复旦大学上海医学院免疫学系 副教授 |
研究重点 | 抗感染免疫 |
教学专著 | 《基础过敏反应学》，科学出版社 (参与) 《医学免疫学》, 复旦大学出版社(参与) |
申请的研究项目 | 国家自然科学基金面上项目No. 31470839 2015-2018.负责人 国家自然科学基金重点项目 No.21334001 2015-2018课题骨干 国家自然科学基金面上项目 No.81072428 2011-2013 负责人 教育部博士点新教师基金 No.20090071120060 2010-2012负责人 上海市科委基础重点项目No.09JC1401800 2009-2011负责人 上海市科委基础重点项目No.10JC1400900 2010-2012 课题骨干 国家自然科学基金面上项目No. 81072409 2011-2013课题骨干 国家自然科学基金重大项目No. 30890140 2009-2012课题骨干 |
承担的实践性教学 | 2008-至今 带教博士、硕士、本科生《医学免疫学》、《细胞与分子免疫学》、《免疫工程》和《疫苗改变世界》 等课程,
担任临床医学八年制导师，指导多名本科生获得“正谊”、“曦源”和“望道”等项目的资助 |
获得的奖励 | 上海市优秀博士学位论文 复旦大学优秀博士学位论文 |
代表性论文 | Reactive Oxygen Species-Mediated c-Jun NH2-Terminal Kinase Activation Contributes to Hepatitis B Virus X Protein-Induced Autophagy via Regulation of the Beclin-1/Bcl-2 Interaction. J Virol. 2017 Jul 12;91(15). pii: e00001-17. (Corresponding author)
Green Tea Polyphenol Epigallocatechin-3-gallate-Alleviated Coxsackievirus B3-induced Myocarditis Through Inhibiting Viral Replication but Not Through Inhibiting Inflammatory Responses. J Cardiovasc Pharmacol. 2017 Jan;69(1):41-47. (Corresponding author)
Blunting Autoantigen-induced FOXO3a Phosphorylation and Degradation Is a Novel Pathway of Glucocorticoids for the Treatment of Systemic Lupus Erythematosus. J Biol Chem.20162016; 291(38):19900-12. ( Corresponding author)
The Defect in Autophagy Induction by Clinical Isolates of Mycobacterium Tuberculosis Is Correlated with Poor Tuberculosis Outcomes. PLoS One 2016;11:e0147810 (Corresponding author)
Epigallocatechin-3-gallate opposes HBV-induced incomplete autophagy by enhancing lysosomal acidification, which is unfavorable for HBV replication. Cell Death Dis 2015;6:e1770 (Corresponding author)
HMGB1 Promotes Systemic Lupus Erythematosus by Enhancing Macrophage Inflammatory Response. J Immunol Res 2015;2015:946748 (Corresponding author)
Inhibition of Histone Deacetylase Activity Aggravates Coxsackievirus B3-Induced Myocarditis by Promoting Viral Replication and Myocardial Apoptosis. J Virol，2015;89:10512-23 (Corresponding author)
Induction of TRIM22 by IFN-γ involves JAK and PC-PLC/PKC, but not MAPKs and pI3K/Akt/mTOR pathways. J Interf Cytok Res, 2013;33(10):578-87 (First author)
Inhibition of histone deacetylase activity suppresses IFN-γ induction of TRIM22 via CHIP-mediated proteasomal degradation of IRF-1. J Immunol, 2013;191(1):464-71 (First author)
p300, but not PCAF, collaborates with IRF-1 in stimulating TRIM22 expression independent of its histone acetyltransferase activity. Eur J Immunol, 2013;43(8):2174-84 (First author)
BRG1 is indispensable for IFN-γ-induced TRIM22 expression, which is dependent on the recruitment of IRF-1. Biochem Biophys Res Commun. 2011; 410; 549–554 (First author)
Identification of tripartite motif-containing 22 (TRIM22) as a novel NF-κB activator. Biochem Biophys Res Commun. 2011; 410; 247–251(First author)
A 5' extended IFN-stimulating response element is crucial for IFN-gamma-induced tripartite motif 22 expression via interaction with IFN regulatory factor-1. J Immunol. 2010;185 (4):2314-23 (First author)
Tripartite motif-containing 22 inhibits the activity of Hepatitis B Virus (HBV) core promoter, which is dependent on nuclear-located RING domain. Hepatology. 2009;50(2):424-33. (First author)
Identification of TRIM22 as a RING finger E3 ubiquitin ligase. Biochem Biophys Res Commun. 2008; 374(3):502-506. (First author) |
联系方式 | Tel: （O）021-54237154； （M）13601639018； E-mail: gaobo@fudan.edu.cn |