标题：蒋争凡
任职
  蒋争凡教授
蒋争凡教授
工作单位： 北京大学 生命科学学院


工作经历
1. 2011-现在，教授/研究员，北京大学-清华大学生命联合中心
2. 2006-现在，教授/研究员，北京大学生命科学学院
3. 2003-2006，Research associate (博士后)，Bruce Beutler’s lab，The Scripps Research Institute, La Jolla, CA, USA
4. 1999-2003，Research associate (博士后) , Xiaoxia Li’s lab & George Stark’s lab, The Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA
5. 1997-1999，博士后，北京大学生命科学学院
教育经历
  蒋老师
1. 1994 - 1997，理学博士，细胞生物学，北京大学
2. 1991 - 1994，理学硕士，细胞生物学，兰州大学
3. 1987 - 1991，理学学士，细胞生物学，兰州大学
执教课程
1. 天然免疫及细胞信号转导（研究生）
2. 细胞生物学进展（研究生）
3. 细胞生物学（本科生）
荣誉
1. 2011年教育部“长江学者”特聘教授
2. 2010年国家杰出青年科学基金
3. 2007年教育部“新世纪优秀人才”
4. 国际细胞因子学会优秀博士后论文一等奖，selected by the International Cytokine Society (ICS)，2002
国内外主要学术组织兼职情况
1、Editor, Scientific Reports（2010-）
2、国家自然科学基金委专家组成员（2010-2013）
3、国家自然科学基金委重大研究计划专家组成员（2010-2017）
科研领域
天然免疫及其相关的细胞信号转导研究天然免疫系统是多细胞生物抵抗病原微生物感染的第一道防线。天然免疫受体通过识别病原体和内源有害分子所特有的分子特征，激活细胞内的一系列信号转导通路，继而引起特异性细胞因子的表达，快速发挥免疫防御作用。同时，天然免疫反应还可以进一步激活获得性免疫反应。天然免疫应答与机体抗病原感染的能力，自身免疫病的发生，过敏性疾病及炎症引起的癌症等密切相关。
本实验室利用多种技术：大规模、高通量克隆表达及功能筛选、规模化酵母双杂交和蛋白质分离-肽谱技术，对调控天然免疫的相关蛋白进行大规模、高通量筛选、克隆及功能研究，寻找并发现天然免疫中调控不同细胞信号通路的新基因及已知基因在天然免疫中的新功能；利用免疫学、细胞生物学、分子生物学、生物化学、遗传学、结构生物学等技术来研究这些基因的功能及作用机制，深入而系统地研究天然免疫反应的分子机制，为相关疾病的预防和治疗提供理论依据。
关键科学问题
围绕细胞受到病原微生物感染后天然免疫激活，并最终产生、分泌细胞因子这一重要生理过程，通过新基因、新通路的发现与机制研究，探讨细胞进行天然免疫反应的分子机制，揭示天然免疫应答失控导致各种与感染免疫相关的疾病，包括过敏性反应、自身免疫病、慢性炎症（及导致肿瘤发生）的可能原因。
1） 细胞识别胞质内病原微生物，激活天然免疫的分子机制；
2） 泛素化参与抗病毒信号通路的机制；
3） 病原微生物感染引发I型干扰素及其它重要细胞因子产生与调控的分子机制；
4） 天然免疫活化后细胞因子分泌的机制；
5） 多种天然免疫系统关键信号转导分子的调节和多种疾病（过敏反应、自身免疫病及慢性炎症）的相互关系，及如何通过瞄准这些分子以达到治疗疾病的目的；
6） 重要信号转导分子的结构及功能。
发表论文
1. Huang YH, Liu XY, Du XX, Jiang Z, Su XD*. 2012, The structural basis for the sensing and binding of cyclic di-GMP by STING. Nat Struct Mol Biol. 19(7):728-30.
2. Zhou X, You F, Chen H, Jiang Z*. 2012, Poly(C)-binding protein 1 mediates house-keeping degradation of mitochondrial antiviral signaling (MAVS). Cell Research. 22 (4): 717-727.
3. Chen H, Sun H, You F, Sun W, Zhou X, Chen L, Yang J, Wang Y, Tang H, Guan Y, Xia W, Gu J, Ishikawa H, Gutman D, Barber G, Qin Z, Jiang Z*. 2011, Activation of STAT6 by STING is Critical for Antiviral Innate Immunity. Cell. 147 (2): 436-446.
4. You FP, Sun H, Zhou X, Sun WX, Liang SM, Zhai ZH, Jiang Z*. 2009, PCBP2 mediates degradation of the adaptor MAVS via the HECT ubiquitin ligase AIP4. Nature Immunology.10: 1300-1308.
5. Sun W, Li Y, Chen L, Chen H, You F, Zhou X, Zhou Y, Zhai Z, Chen D, Jiang Z*. 2009, ERIS, an ER IFN stimulator, activates innate immune signaling through dimerization. Proc Natl Acad Sci USA. 106 (21): 8653-8.
6. Xiao H, Qian W, Staschke K, Qian Y, Cui G, Deng L, Ehsani M, Wang X, Qian YW, Chen ZJ, Gilmour R, Jiang Z*, Li X*. 2008, Pellino 3b negatively regulates interleukin-1-induced TAK1-dependent NFkB activation. J Biol Chem. 283(21):14654-64.
7. Jiang Z, Georgel P, Li C, Choe J, Crozat K, Rutschmann S, Du X, Bigby T, Mudd S, Sovath S, Wilson IA, Olson A, Beutler B. 2006, Details of Toll-like receptor:adapter interaction revealed by germ-line mutagenesis. Proc Natl Acad Sci USA. 103 (29): 10961-66.
8. Jiang Z, Georgel P, Du X, Shamel L, Sovath S, Mudd S, Huber M, Kalis C, Keck S, Galanos C, Freudenberg M, Beutler B. 2005, CD14 is required for MyD88-independent LPS signaling. Nature Immunology. 6(6): 565-70.
9. Jiang Z, Mak TW, Sen G, Li X. 2004, Toll-like receptor 3-mediated activation of NF-kappaB and IRF3 diverges at Toll-IL-1 receptor domain-containing adapter inducing IFN-beta. Proc Natl Acad Sci USA. 101(10): 3533-8.
10. Jiang Z, Zamanian-Daryoush M, Nie H, Silva AM, Williams BR, Li X. 2003 Poly (IC)-induced TLR3-mediated activation of NFkappa B and MAP kinase is through an IRAK-independent pathway employing the signaling components TLR3-TRAF6-TAK1-TAB2-PKR. J Biol Chem. 278(19): 16713-9.
11. Jiang Z, Johnson HJ, Nie H, Qin J, Bird TA, Li X. 2003, Pellino 1 is required for interleukin-1 (IL-1)-mediated signaling through its interaction with the IRAK4-IRAK-TRAF6 complex. J Biol Chem. 278(13): 10952-6.
12. Jiang Z,Ninomiya-Tsuji J, Qian Y, Matsumoto K, Li X. 2002, Interleukin-1 (IL-1) receptor-associated kinase-dependent IL-1-induced signaling complexes phosphorylate TAK1 and TAB2 at the plasma membrane and activate TAK1 in the cytosol. Mol Cell Biol. 22(20): 7158-67.
13. Beutler B,Jiang Z,Georgel P, Crozat K, Croker B, Rutschmann S, Du X and Hoebe K, 2006, Genetic Analysis of Host Resistance: Toll-like Receptor Signaling and Immunity at Large. Annual Review of Immunology 24: 353-89.
14. Qian Y, Zhao Z,Jiang Z, Li X. 2002, Role of NF kappa B activator Act1 in CD40-mediated signaling in epithelial cells. Proc Natl Acad Sci USA. 99(14): 9386-91.
15. Li X, Commane M, Jiang Z, Stark GR. 2001, IL-1-induced NFkB and JNK activation diverge at IRAK. Proc Natl Acad Sci USA. 98(8): 4461-5.
16. Jiang Z, Hong X, Long H, Zhai ZH, 2000, Ceramides induce apoptosis in Hela cells and enhance cytochrome c-induced apoptosis in Xenopus egg extracts. Cell Mol Life Sci. 57(7): 1117-25.
17. Schabbauer G, Luyendyk J, Crozat K,Jiang Z, Mackman N, Bahram S, Georgel P. 2008, TLR4/CD14-mediated PI3K activation is an essential component of interferon -dependent VSV resistance in macrophages. Mol Immunol. 45(10):2790-6.
18. M. Otsuka, Q. Jing, P. Georgel, New, J. Chen, J. Mols, Y.J. Kang, Z. Jiang, S. C. Das, A. K. Pattnaik, J. Carlos dela Torre, B. Beutler and J. Han. 2007, Hypersusceptibility to vesicular stomatitis virus infection in Dicer-deficient mice is due to impaired miR24 and miR93 expression. Immunity, 27: 123-134.
19. Yao J, Kim TW, Qin J, Jiang Z, Qian Y, Xiao H, Lu Y, Qian W, Gulen MF, Sizemore N, DiDonato J, Sato S, Akira S, Su B, Li X. 2007, Interleukin-1 (IL-1)-induced TAK1-dependent Versus MEKK3-dependent NFkB activation pathways bifurcate at IRAK modification. J Biol Chem. 282(9):6075-89.
20. Jin G, Klika A, Callahan M, Faga B, Danzig J, Jiang Z, Li X, Stark GR, Harrington J, Sherf B. 2004, Identification of a human NFkB-activating protein, TAB3. Proc Natl Acad Sci USA. 101(7): 2028-33.
21. Georgel P, Jiang Z, Kunz S, Janssen E, Mols J, Hoebe K, Bahram S, Oldstone MB, Beutler B. 2007, Vesicular stomatitis virus glycoprotein G activates a specific antiviral Toll-like receptor 4-dependent pathway. Virology 362(2): 304-313.
22. Huber M, Kalis C, Keck S, Jiang Z, Georgel P, et al. 2006 R-form LPS, the master key to the activation of TLR4/MD-2-positive cells. Eur J Immunol. 36: 701-11.
23. Hoebe K.Jiang Z,George P, Tabeta K, Janssen E, Du X, and Beutler B. 2006, TLR signaling pathways: opportunities for activation and blockade in pursuit of therapy. Current Pharmaceutical Design 12: 4123-34.
24. Georgel P, Crozat K, Lauth X, Makrantonaki E, Seltmann H, Sovath S, Hoebe K, Du X, Rutschmann S, Jiang Z, Bigby T, Nizet V, Zouboulis CC, Beutler B. 2005, A toll-like receptor 2-responsive lipid effector pathway protects mammals against skin infections with gram-positive bacteria. Infect Immun. 73: 4512-21.
25. Hoebe K, Jiang Z, Tabeta K, Du X, Georgel P, Crozat K, Beutler B. 2006, Genetic analysis of innate immunity. Adv immunol. 91: 175-226.
26. Beutler B, Georgel P, Rutschmann S, Jiang Z, Croker B, Crozat K. 2005, Genetic analysis of innate resistance to mouse cytomegalovirus (MCMV). Brief Funct Genomic Proteomic. 4:203-13. Review.
27. Zhou Z, Hoebe K, Du X, Jiang Z, Shamel L, Beutler B. 2005, Antagonism between MyD88- and TRIF-dependent signals in B7RP-1 up-regulation. Eur J Immunol. 35 (6): 1918-27.
28. Qin J, Jiang Z, Qian Y, Casanova JL, Li X. 2004, IRAK4 kinase activity is redundant for interleukin-1 (IL-1) receptor-associated kinase phosphorylation and IL-1 responsiveness. J Biol Chem. 279(25): 26748-53.
29. Silva AM, Whitmore M, Xu Z, Jiang Z, Li X, Williams BR. 2004, Protein kinase R (PKR) interacts with and activates mitogen-activated protein kinase kinase 6 (MKK6) in response to double-stranded RNA stimulation. J Biol Chem. 279(36): 37670-6.
30. Nguyen H, Chatterjee-Kishore M, Jiang Z, Qing Y, Ramana CV, Bayes J, Commane M, Li X, Stark GR. 2003, IRAK-dependent phosphorylation of Stat1 on serine727 inresponse to IL-1 and effects on gene expression. J Interferon Cytokine Res. 23 (4): 183-92.[1]