Research Focus:
Main research directions (not limited to):
1. Tumor immunity: using CRISPRn/i/a (knocking out, inhibition or activation of target genes) technology, combined with the corresponding whole genome library or functional single sgRNA (double sgRNA) sublibrary, using in vivo tumorigenic models to study:
(1) the molecular mechanism of tumor cell metastasis to lymph nodes;
(2) Molecular mechanisms by which tumor cells escape the immune system;
(3) The molecular mechanism of infiltration, activation (inactivation) of various types of immune cells in the tumor microenvironment.
2. The function of intestinal microbiome in gastrointestinal diseases: using the CRISPR high-throughput screening platform,
(1) identify the target of pathogenic bacteria acting on host cells;
(2)analyze the molecular mechanism of host cell response to pathogenic bacteria;
(3) Explore the interaction mechanism of intestinal microbiome, intestinal immunity, intestinal nerves and intestinal cells.
3. Tumor radiotherapy and chemotherapy tolerance: Using the CRISPRn/i/a screening system, combined with tumorigenic models (such as brain tumor, bowel cancer, liver cancer) in mice in vivo, the genes that regulate tumor cells' tolerance to different anti-tumor drugs (or targeted therapy drugs) or radiotherapy tolerance under different genetic backgrounds were analyzed, and the molecular mechanism was elucidated.
4. Conducive to the targeted localization function of CRISPR tools, the analysis of the epigenetic regulatory mechanism of gene expression, the genetic interaction between functional DNA elements, and the high-level structure, function and dynamic regulatory mechanism of the genome.
5. Explore the molecular mechanisms by which tumors cause pain.
Educational background:
1998~2002: Bachelor of Science in Biochemistry, Department of Biochemistry, Nanjing University;
2002~2009: Ph.D. in Biochemistry and Molecular Biology, Shanghai Institute of Biochemical Cells, Chinese Academy of Sciences;
2005.3~2005.12: Visiting Ph.D., Max Planck Institute of Biochemistry, Germany;
2006.1~2006.4: Visiting Ph.D., Institute of Molecular Pathology, Copenhagen, Denmark;
Work experience:
2009~2010：Research Assistant, Shanghai Institute of Biochemical Cells, Chinese Academy of Sciences;
2010~2015：Postdoctoral Fellow, Department of Cell and Histology, University of California, San Francisco;
2015~2018：Associate Specialist, Department of Cell and Histology, University of California, San Francisco;
2014.10~2015.3 Visiting scholar, Department of Bioengineering, Stanford University;
2015.5~2017.4: Visiting scholar, Gladstone Institute, USA;
Selected Publications
1. Dan Du#, Yoko Katsuno, Dominique Meyer, Erine H. Budi, Si-Han Chen, Hongjun Wang, Hartmut Koeppen, Rosemary Akhurst, Rik Derynck#. Smad3‐mediated recruitment of the methyltransferase SETDB1/ESET controls Snail1 expression and epithelial–mesenchymal transition. EMBO Reports., 2017 Dec 12th; 19(1), 135-155 (#: co-corresponding author);
2. Dan Du*, Assen, Roguev*, David E Gordon，Meng Chen, Si-Han Chen, John Paul Shen, Prashant Mali, Trey Ideker, Stanley Qi, Nevan Krogan. Genetic interaction mapping in mammalian cells using CRISPR interference. Nat. Methods., 2017 May 8th; 14(6), 577–580 (*: co-first author)；
3. Dan Du, Feilai Xu, Lihou Yu, Chenyi Zhang, Xuefeng Lu, Haixin Yuan, Qin Huang, Fan Zhang, Xunwei Wu, Zhe Zhang, Xueliang Zhu, Xiaohui Zhang, Zhengjun Chen. Tight junction protein occludin regulates directional migration of epithelial cells. Dev Cell., 2010 Jan 19th, 18 (1), 52-63；
4. Dan Du, Stanley Qi. CRISPR Technology for Genome Activation and Repression in Mammalian Cells. Cold Spring Harb Protoc. 2016 Jan 4th; (1), pdb. prot090175；
5. Dan Du, Stanley Qi. An Introduction to CRISPR Technology for Genome Activation and Repression in Mammalian Cells. Cold Spring Harb Protoc. 2016 Jan 4th ; (1), pdb. top086835；
6. Dan Du, Esben Pedersen, Zhipeng Wang, Richard Karlsson, Zhengjun Chen, Xunwei Wu, Cord Brakebusch. (2009) Cdc42 is crucial for the maturation of primordial cell junctions in keratinocytes independent of Rac1. Exp Cell Res., 315, 1480-1489.
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