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教授
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韩家淮
发布时间: 2022年01月06日浏览次数:



韩家淮 HAN Jiahuai, Ph.D.

教授,中国科学院院士,博士生导师

话:0592-2189390

E-mail:jhan@xmu.edu.cn

实验室网址:http://hanlab.xmu.edu.cn/

                      (请访问实验室网站,获取最新信息)


1978-1982
年,北京大学学士学位;

1982-1985年,北京大学硕士学位;

1990年,比利时布鲁塞尔大学,博士学位;

19901992年,美国德克萨斯大学西南医学中心博士后;

19932007年,历任美国Scripps研究所助理教授、副教授、教授;

20011120077月,兼任我校特聘教授;

20078月至今,我校生命科学学院教授;

2013年12月,中国科学院院士;

我校医学与生命科学学部主任; 

细胞应激生物学国家重点实验室主任;

我校实验动物中心主任; 

我校副校长。

1978-1982, Beijing University (Peking University), China, B.S., Specialty in Biochemistry

1982-1985, Beijing University (Peking University), China, M. S., Specialty in Protein Chemistry

1985-1990,University of Brussels (Université Libre de Bruxelles), Belgium, 1990, Ph.D., Specialty in Molecular  Biology

1990-1992, Research Fellow, Department of Internal Medicine and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA

1992-1993, Research Associate, Department of Immunology, The Scripps Research Institute,La Jolla, California,  USA

1993-1996, Assistant Member, Department of Immunology, The Scripps Research Institute,La Jolla, California,  USA

1996-2004, Associate Professor, Department of Immunology, The Scripps Research Institute,La Jolla, California,  USA

 2004-2007, Professor, Department of Immunology, The Scripps Research Institute,La Jolla, California, USA

 2002- 2007,Adj. Professor, School of Life Sciences, Xiamen University, Xiamen, China

 2007 to present, Professor, School of Life Sciences, Xiamen University, Xiamen, China

 Dean, Faculty of Medicine and Life Sciences, Xiamen University, China


 Director, State Key Laboratory of Cellular Stress Biology

 Director,Innovation Center for Cell Signaling Network

 Director,Laboratory Animal Center,Xiamen University,China

 Vice President,Xiamen University,Xiamen,China


研究领域(Research Area)

本实验室主要关注细胞应激反应在生理病理过程中的作用。主要用大规模基因突变和基因敲除的方法寻找关键的基因,并在细胞水平和两种模式生物——小鼠和果蝇上进行验证。然后分析这些基因及它们所介导的信号通道在应激反应中的作用。

  细胞应激反应(Cellular Stress responses)是细胞对不同的环境压力所产生的共同反应。外界感染以及内部病变所引起的应激反应是免疫炎症的重要组成部分,在许多人类重大疾病如肿瘤的发生发展中起着非常重要的作用。

细胞应激反应涉及很多生理过程,我们拟解决以下问题:

1.细胞应激反应在细胞分化、细胞衰老、细胞凋亡和坏死的关系

2.细胞应激反应和细胞癌变相关信号通路的关系

3.细胞应激反应和肿瘤细胞代谢通路的关系

4.免疫炎症和动脉粥样硬化、脓血症、肠炎与肠癌这些疾病的关系

      Our research interests are the molecular mechanisms incellular stress responses including inflammation and inflammation related diseases. Specifically, we are interested in:

       1.The relationship betweencellular stress responses and cell differentiation, senescence and death.

       2.The relationship betweencellular stress responses and malignancy.

       3.The relationship betweencellular stress responses and metabolic pathways.

       4.The functions ofcellular stress response pathways in septic shock, atherosclerosis, colitis and other

inflammation related disease.


代表性论文(Selected Publications)

1. He WT, Wan H, Hu L, Chen P, Wang X, Huang Z, Yang ZH,Zhong CQ,Han J.Gasdermin D is an executor ofpyroptosis and required for interleukin-1βsecretion. Cell Res. 2015 Dec; 25(12): 1285-98.

2. Li Y,Zhong CQ, Xu X,Cai S, Wu X, Zhang Y, Chen J, Shi J, Lin S,Han J. Group-DIA: analyzing multiple data-independent acquisition mass spectrometry data files. Nat Methods. 2015 Oct 5;12(12):1105-6.

3. Chen W, Wu J, Li L, Zhang Z, Ren J, Liang Y, Chen F, Yang C, Zhou Z, Sean Su S, Zheng X, Zhang Z,Zhong CQ, Wan H, Xiao M, Lin X, Feng XH,Han J. Ppm1b negatively regulates necroptosis through dephosphorylating Rip3. Nat Cell Biol. 2015; 17(4): 434-444.

4.Huang Z, Wu SQ, Liang Y, Zhou X, Chen W, Li L, Wu J, Zhuang Q, Chen C, Li J,Zhong CQ, Xia W, Zhou R, Zheng C,Han J. RIP1/RIP3 Binding to HSV-1 ICP6 Initiates Necroptosis to Restrict Virus Propagation in Mice. Cell Host & Microbe. 2015 ; 17(2): 229-42.

5.Chen X, Li W, Ren J, Huang D, He WT, Song Y, Yang C, Li W, Zheng X, Chen P,Han J. Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death. Cell Res. 2013; 24(1):105-21.

6. Zhang DW,Shao J, Lin J, Zhang N, Lu BJ, Lin SC, Dong MQ, Han J. 2009. RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis. Science325: 332-6

7.  Sun P,Yoshizuka N, New L, Moser BA, Li Y, Liao R,Xie C, Chen J, Deng Q,Yamout M, Dong MQ,Frangou CG, Yates JR, 3rd, Wright PE, Han J. 2007. PRAK is essential forras-induced senescence and tumor suppression. Cell128: 295-308

8. Jing Q, Huang S,Guth S,Zarubin T,Motoyama A, Chen J, DiPadova F, Lin SC, Gram H, Han J. 2005. Involvement ofmicroRNA in AU-rich element-mediated mRNA instability.Cell120: 623-34

9.Ge B, Gram H, DiPadova F, Huang B, New L,Ulevitch RJ,Luo Y, Han J. 2002. MAPKK-independent activation of p38alpha mediated by TAB1-dependentautophosphorylation of p38alpha. Science295: 1291-4 

10. Han J, Jiang Y, Li Z,Kravchenko VV,Ulevitch RJ. 1997. Activation of the transcription factor MEF2C by the MAPkinase p38 in inflammation. Nature386: 296-9 

11. Han J, Lee JD,Bibbs L,Ulevitch RJ. 1994. A MAPkinase targeted byendotoxin andhyperosmolarity in mammalian cells. Science265: 808-11



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