师资队伍
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       我们在北京生命科学研究所(NIBS)的研究目标是阐明细胞死亡的分子机理。我们相信这些知识将帮助我们理解现代社会中包括癌症、自身免疫疾病、心血管疾病以及神经退行性疾病等主要疾病的发病机理,并进而有助我们设计出相应的治疗策略。我们目前的研究是过去15年来对细胞凋亡,一种由细胞内的Caspases执行的细胞死亡形式的系统研究的延伸。这些研究经历使我们认识到细胞凋亡仅仅只是细胞自我灭亡的形式之一,另外还有一些细胞死亡的其它方式,它们通过与细胞凋亡相似而又不同的细胞内成份和调节机制来完成。这其中包括我们目前注意到的由肿瘤坏死因子受体诱发的细胞坏死。我们发现了一种在肿瘤坏死因子受体下游的激酶Rip3在这种细胞死亡形式中起着关键作用。我们正在研究Rip3是如何杀死细胞,以及这个过程与细胞凋亡以及其它形式的细胞死亡间有何联系。                                

       我们在北京生命科学研究所(NIBS)的研究目标是阐明细胞死亡的分子机理。我们相信这些知识将帮助我们理解现代社会中包括癌症、自身免疫疾病、心血管疾病以及神经退行性疾病等主要疾病的发病机理,并进而有助我们设计出相应的治疗策略。我们目前的研究是过去15年来对细胞凋亡,一种由细胞内的Caspases执行的细胞死亡形式的系统研究的延伸。             

The goal of our research laboratory at the National Institute of Biological Sciences (NIBS), Beijing is to understand cell death at molecular level.   The research scope is an expansion of our previous 15 years of research focus on apoptosis, a form of cell death executed by intracellular caspases.  These research experiences brought us to realization that apoptosis is only one form of self-disruptive cell death; and many forms of cell death share cellular components and regulators with apoptotic machinery.  One form of cell death that recently brought to our attention is the tumor necrosis factor receptor induced cell death when caspases are inhibited. We discovered that a receptor interactive kinase, Rip3, is a critical downstream mediator for this form of cell death.  We are in the process of studying how Rip3 kills a cell.


The goal of our research laboratory at the National Institute of Biological Sciences (NIBS), Beijing is to understand cell death at molecular level.   The research scope is an expansion of our previous 15 years of research focus on apoptosis, a form of cell death executed by intracellular caspases.  These research experiences brought us to realization that apoptosis is only one form of self-disruptive cell death; and many forms of cell death share cellular components and regulators with apoptotic machinery.  One form of cell death that recently brought to our attention is the tumor necrosis factor receptor induced cell death when caspases are inhibited. We discovered that a receptor interactive kinase, Rip3, is a critical downstream mediator for this form of cell death.  We are in the process of studying how Rip3 kills a cell.