• Man Mohan


    一、教育和工作经历Education and Work Experience




    1998年07月–2000年05月,印度Devi Ahilya大学,生命科学,硕士



    04-2013 -12-2019, Professor, Shanghai Jiao Tong University School of Medicine

    03-2008 - 03-2013, Post Doctoral Research Associate, Stowers Institute for Medical Research, Kansas City, USA

    06-2004 - 12-2007, Justus Liebig University, Giessen, Germany, PhD

    07-1998 - 05-2000, Master of Sciences, Devi Ahilya Vishwavidyalaya, Indore, India

    07-1994 - 05-1997 Bachelor of Sciences, University of Delhi, New Delhi, India

    二、主要研究方向Main Research Directions

    1. Chromosomal translocations and leukemia.
    2. Functional analysis of DYRK1A to unravel its role in leukemia and in neurodegenerative disease.
    3. Development of Biochemical research platform for large scale protein production.
    4. Development of primate models of human diseases.

    三、科研领域描述Description of Scientific Research

    Chromosomal translocations that fuse mixed lineage leukemia 1 (MLL1) to any one of a large number of translocation partners are indicative of a poor clinical outcome in acute myeloid and lymphoid leukaemias. Up to 90% of infant leukemias bear MLL-translocations to either of the ~100 fusion gene partners. In these leukemias, MLL-fusion proteins are thought to confer biochemical activities, which promote the transcription of leukemogenic transcriptional program, including expression of HOX A9 genes, thus causing leukemia. We are investigating novel functions of the MLL-fusion proteins to understand how they cause leukemia.


    Down syndrome is one of the most common genetic diseases caused by chromosomal abnormalities, including Nondisjunction, mosaicism and chromosomal translocation. DYRK1A, a gene located in Down Syndrome Critical Region on chromosome 21, is considered an important effector of some Down syndrome phenotypes. We are trying to unravel the molecular functions of DYRK1A in cellular physiology and neuronal system, using proteomics, genomics, and mouse models.

    四、承担科研项目情况Research Projects

    1. 国家自然科学基金面上项目,31471206,DOT1L介导的H3K79甲基化机制,2015/01-2018/12,90万元,在研,主持
    2. 上海市东方学者(特聘教授),2015年,基础医学

    五、代表论文Representative papers 

    1. Xu S, Zhan M, Jiang C, He M, Yang L, Shen H, Huang S, Huang X, Lin R, Shi Y, Liu Q, Chen W, Mohan M, Wang J. Genome-wide CRISPR screen identifies ELP5 as a determinant of gemcitabine sensitivity in gallbladder cancer. Nat Commun. 2019 Dec 2;10(1):5492.
    2. Shen H, He M, Lin R, Zhan M, Xu S, Huang X, Xu C, Chen W, Yao Y, Mohan M*, Wang J. *. PLEK2 promotes gallbladder cancer invasion and metastasis through EGFR/CCL2 pathway. J Exp Clin Cancer Res. 2019 Jun 10;38(1):247. doi: 10.1186/s13046-019-1250-8  * Co-corresponding author
    3. Li S, Xu C, Fu Y, Lei PJ, Yao Y, Yang W, Zhang Y, Washburn MP, Florens L, Jaiswal M, Wu M, Mohan Man*. DYRK1A interacts with Histone Acetyl Transferase p300 and CBP and localizes to enhancers.. Nucleic Acids Res. 2018 Nov 30;46(21):11202-11213  *Corresponding author
    4. Wang H, Zhan M, Xu SW, Chen W, Long MM, Shi YH, Liu Q, Mohan M, Wang J. miR-218-5p restores sensitivity to gemcitabine through PRKCE/MDR1 axis in gallbladder cancer. Cell Death Dis. 2017 May 11;8(5):e2770.
    5. Rickels R, Hu D, Collings CK, Woodfin AR, Piunti A, Mohan M, Herz HM, Kvon E, Shilatifard A. An Evolutionary Conserved Epigenetic Mark of Polycomb Response Elements Implemented by Trx/MLL/COMPASS. Mol Cell. 2016, Jul 21;63(2):318-28
    6. Mohan M, Herz HM, Shilatifard A. “SnapShot: Histone Lysine Methylase Complexes” Cell. 2012 149, April 13.
    7. Herz HM, Mohan M, Garruss AS, Liang K, Takahashi YH, Mickey K, Voets O, Verrijzer CP, Shilatifard A. Enhancer-associated H3K4 monomethylation by Trithorax-related, the Drosophila homolog of mammalian Mll3/Mll4. Genes Dev 2012 Dec 1;26(23):2604-20
    8. Mohan M, Herz HM, Smith ER, Zhang Y, Jackson J, Washburn MP, Florens L, Eissenberg JC, Shilatifard A. “The COMPASS family of H3K4 methylases in Drosophila.” Mol Cell Biol. 2011 Nov;31(21):4310-8.
    9. Mohan M, Lin C, Guest E, Shilatifard A. “Licensed to elongate: a molecular mechanism for MLL-based leukemogenesis.” Nat Rev Cancer. 2010 Oct;10(10):721-8.
    10. Mohan M, Herz HM, Takahashi YH, Lin C, Lai KC, Zhang Y, Washburn MP, Florens L, Shilatifard A.  “Linking H3K79 trimethylation to Wnt signaling through a novel Dot1-containing complex (DotCom)” Genes & Dev 2010 Mar 15;24(6):574-89