科学研究

黄志伟:

研究领域

我们实验室的主要研究内容:

一、研究免疫与感染性疾病领域的重要生物大分子的结构和功能的关系。我们对膜上参与细胞信号转导的GPCR受体/配体复合物,以及重要病原如HIV与宿主相互作用的蛋白及其复合物的结构与功能的关系进行研究。

二、研究CRISPR-Cas系统对入侵核酸片段获取、整合以及剪切的分子机制。CRISPR-Cas系统是细菌和古细菌用来抵御病毒等外来入侵者的适应性免疫反应系统。我们对各类型的CRISPR-Cas系统的工作机制进行研究,同时基于研究成果靶向设计高效的、特异性的基因编辑工具。

三、病原感染引发的细胞死亡的分子机制研究。HIV等病原体感染导致细胞死亡,我们希望通过对受感染细胞发生死亡的机制进行研究找出jkjkjdfsfgdfg参与该信号途径的重要分子和分子事件。

我们采用整合的研究方法对感兴趣、且具有重要意义的课题进行研究,这一系列研究手段包括病毒学、结构生物学、分子细胞生物学以及小鼠遗传学等。将结构与体内外功能研究密切结合,从分子、细胞以及个体水平等多个层次,以较全视野研究目标蛋白质(复合物)分子结构和功能,及其信号调控机制。

除了上述结构生物学及信号通路方面的基础研究外,我们也对免疫与感染性疾病发生过程中起关键作用的可溶/膜蛋白(复合物)的结构进行解析,并利用这些结构信息理性设计小分子药物治疗上述疾病。


招聘该研究组现招聘副教授、博士后、技术员

欢迎有大分子X射线晶体学、冷冻电镜、HIV病毒学、免疫学、基因编辑等研究背景的人员申请。也欢迎有其它研究背景,如病原微生物学,细胞生物学,生物物理学或物理学博士学位,且对生命科学研究有强烈兴趣的人员申请。该实验室根据个人研究背景提供薪资待遇。请申请者将一份CV、以及三位推荐人的联系方式发至huangzhiwei2009@gmail.com

发表文章:( *  Co-first author,  # Corresponding  author

  1. Pu Gao,  Hui Yang, Kanagalaghatta R Rajashankar, Zhiwei Huang and  Dinshaw J Patel (2016). Type V CRISPR-Cas Cpf1 endonuclease employs a unique  mechanism for crRNA-mediated target DNA recognition. Cell  Research. 26, 901–913.

  2. De  Dong*, Kuan Ren*, Xiaolin Qiu*, Jianlin Zheng, Minghui Guo, Xiaoyu Guan, Hongnan  Liu, Ningning Li, Bailing Zhang, Daijun Yang, Chuang Ma, Shuo Wang, Dan Wu,  Yunfeng Ma, Shilong Fan, Jiawei Wang, Ning Gao and Zhiwei Huang#  (2016). Crystal structure of CRISPR-Cpf1 in complex with CRISPR  RNA (crRNA). Nature. 532,  522-526.  (This paper is highlighted in Nature Reviews  Microbiology (2016), and Nature Structural &  Molecular Biology, 23, 365-366 (2016))

  3. Yingying  Guo*, Liyong Dong*, Xiaolin Qiu*, Yishu Wang, Bailing Zhang, Hongnan Liu, You  Yu, Yi Zang, Maojun Yang and Zhiwei Huang#  (2014). Structural basis for hijacking CBF-β and CUL5 E3  ligase complex by HIV-1 Vif. Nature. 505,  229-233. (This paper is featured with News & Views, Nature. 505,  167-168, highlighted in Nature Structural & Molecular  Biology, 21, 117 (2014))

  4. Jae-Hyuck  Shim, Matthew B. Greenblatt, Weiguo Zou, Zhiwei Huang, Marc N.  Wein, Nicholas Brady, Dorothy Hu, Jean Charron, Heather R. Brodkin, Gregory A.  Petsko, Dennis Zaller, Bo Zhai, Steven Gygi, Laurie H. Glimcher and Dallas C.  Jones (2013). Schnurri-3 regulates ERK downstream of WNT signaling in  osteoblasts. J Clin  Invest. doi:10.1172/JCI69443.

  5. Zehan  Hu, Chuangye Yan, Peiyuan Liu, Zhiwei Huang, Rui Ma, Chenlu  Zhang, Ruiyong Wang, Yueteng Zhang, Fabio Martinon, Di Miao, Haiteng Deng,  Jiawei Wang, Junbiao Chang, Jijie Chai (2013). Crystal structure of NLRC4  reveals its autoinhibition mechanism. Science. 12,  172-175.

  6. Weiguo  Zou, Xi Chen, Jae Shim, Zhiwei Huang, Nicholas  Brady, Dorothy Hu, Rebecca Drapp, Kirsten Sigrist, Laurie H. Glimcher, Dallas  Jones (2011). The E3 ubiquitin ligase Wwp2 regulates craniofacial development  through monoubiquitination of Goosecoid. Nature Cell  Biology. 13, 59-65.

  7. Chen  D, Lei L, Flores R, Zhiwei  Huang, Wu Z, Chai J, Zhong G. (2010). Autoprocessing and  self-activation of the secreted protease CPAF in Chlamydia-infected cells.  Microbial  Pathogene­sis. 1(10), 1-10.

  8. Zhiwei  Huang and  Jijie Chai (2010). Mapping the selection mechanisms by bacterial GEFs.  Virulence. 1(2),  1-4.

  9. Zhiwei  Huang*,  Sarah E. Sutton*, Adam J. Wallenfang, Robert C. Orchard, Xiaojing Wu, Yingcai  Feng, Jijie Chai and Neal M. Alto (2009). Structural insights into host GTPase  isoform selection by a family of bacterial GEF mimics. Nature Structural & Molecular  Biology. 16(8), 853 – 860. (This publication was selected  as cover story, and high­lighted by Nature China

  10. Zhiwei  Huang,  Yingcai Feng, Ding Chen, Xiaojing Wu, Xiaojun Wang, Xingguo Xiao, Wenhui Li, Niu  Huang, Lichuan Gu, Guangming Zhong and Jijie Chai (2008). Structural basis for  activation and inhibition of the secreted chlamydia protease CPAF.  Cell Host &  Microbe. 4(6), 529-542. (This publication was selected as a  research “highlight” by Nature China

  11. Maikke  B. Ohlson, Zhiwei  Huang, Neal M. Alto, Jack E. Dixon, Jijie Chai and Samuel I.  Miller (2008). Structure and Function of Salmonella SifA Indicate that Its  Interactions with SKIP, SseJ, and RhoA Family GTPases Induce Endosomal  Tubulation. Cell Host  & Microbe. 4(5), 434-446.