首页 全所PI名录
  • 姜海
  • 研究员,研究组长,博士生导师
  • E-mail: hai@@sibcb.ac.cn
  • 实验室主页: 
    个人简介:
  •   2011年-至今:中国科学院上海生命科学研究院生物化学与细胞生物学研究所,研究员,研究组长

      2007-2011年:美国麻省理工学院癌症研究中心,博士后

      2000-2006年:美国西北大学医学院,博士

      1996-2000年:北京大学生命科学学院,学士

    社会任职:
    研究方向:
  • 肿瘤靶标和药物筛选
    研究工作:
  • 癌症是由多种基因突变造成的恶性疾病。大规模癌症基因组研究使我们对癌症有了更加深入的认识,然而仍有一些关键问题亟待解决。一些基因型的肿瘤缺乏可用的治疗靶点,此外,许多靶点属于传统药物模式下的“不可成药”靶点。我们在以下几个方向开展研究,以拓展靶向治疗。

    1) 肿瘤中新治疗靶点的发现。通过全基因组CRISPR筛选,对经典的癌症相关信号通路如Wnt、TGF、VHL-HIF等进行深度研究,发现这些通路的新的重要调控基因,其中的一些可为肿瘤提供治疗靶点。此外,我们还利用全基因组CRISPR筛选技术,全面分析决定各类药物抗癌活性的最重要基因。相关结论可为各类抗癌药物的精准使用提供生物标志物,也可为这些药物提供合成致死靶点,从而改善药物的治疗效果。

    2) 许多重要疾病的驱动蛋白属于“难以成药”靶点,对应了非常大的未满足患者需求。针对这类靶点的分子胶降解剂是生物医学领域的研究热点和药物研发的重点方向。我们创立了新型高通量降解剂筛选体系,对各类疾病的重要靶点蛋白开展降解剂筛选并进行后续研究,为这些“难以成药”靶点提供新的候选靶向药物。

    承担科研项目情况:
    代表论著:
    1. Fan P, Shang XY, Song A, Chen S, Mao RY, Ma J, Chen J, Wang Z, Zheng H, Tao B, Hong L, Liu J, XU W, W Jiang, H Shen, Zhang Q, Yang H, Meng XM, Lan F, Cheng J, Xu C, Zhang P*, Jiang H*, Chen F*. Catalytic-independent functions of Integrator/INTAC confer sensitivity to BET inhibition. (2024) Nature Chemical Biology Accepted (* Co-corresponding author)
    2. Zhao Y, Jiang W, Gao H, Pan G, Wu Y, Wang Y, Sheng M, Xie J, Wu W, JI Z, Du Y, Zhang L, Wang X, Walsh CP, Jiang H*, Xu G*, Zhou D*. DCK confers sensitivity of DCTD-positive cancer cells to oxidized methylcytidines. (2023) Protein & Cell 14(7):532-537. (* Co-corresponding author)
    3. He Z, Li R, Jiang H. Mutations and Copy number abnormalities of hippo pathway components in human cancers. (2021) Frontiers in Cell and Developmental Biology, 2021 Jun 3;9:661718
    4. Xu L, Li P, Hao X, Lu Y, Liu M, Song W, Shan L, Yu J, Ding H, Chen S, Yang A, Zeng YA, Zhang L*, Jiang H*. SHANK2 is a frequently amplified oncogene with evolutionarily conserved roles in regulating Hippo signaling. (2021) Protein & Cell 12(3):174-193. (* Co-corresponding author)
    5. Shan L, Yu J, He Z, Chen S, Liu M, Ding H, Xu L, Zhao J, Yang A, Jiang H. Defining relative mutational difficulty to understand cancer formation. (2020) Cell Discovery Jul 21;6:48.
    6. Jiang H. The expanding vulnerabilities of being UTXless. (2019) Signal Transduction and Targeted Therapy. 4:12
    7. Ding H, Zhao J, Zhang Y, Yu J, Liu M, Li X, Xu L, Lin M, Liu C, He Z, Chen S, Jiang H. Systematic analysis of drug vulnerabilities conferred by tumor suppressor loss. (2019) Cell Reports 27(11):3331-3344 (Recommended by Faculty of 1000)
    8. Li X, Zhang Y, Zheng L, Liu M, Chen CD, Jiang H. UTX is an escape from X-inactivation tumor-suppressor in B cell lymphoma. (2018) Nature Communications. 9(1):2720.
    9. Liu C, Ding H, Li X, Pallasch CP, Hong L, Guo D, Chen Y, Wang D, Wang W, Wang Y*, Hemann MT*, Jiang H*. A DNA/HDAC dual-targeting drug with significantly enhanced anticancer potency. (2015) EMBO Molecular Medicine, 7(4):438-49 (*Corresponding author)
    10. Wang N, Ding H, Liu H, Li X, Wei L, Yu J, Liu M, Ying M, Gao W, Jiang H* , Wang Y*. A novel recurrent CHEK2 Y390C mutation identified in high risk Chinese breast cancer patients impairs its activity and is associated with increased breast cancer risk. (2015) Oncogene, 34(40):5198-205 (*Corresponding author)
    11. Wu J#, Jiang H#, Luo S#, , Zhang M, Zhang Y, Sun F, Huang S and Li H. Caspase-mediated cleavage of C53/LZAP protein causes abnormal microtubule bundling and rupture of the nuclear envelope. (2013) Cell Research, 23(5):691-704. (#equal contribution)
    12. Jiang H, Pritchard JR, Williams RT, Lauffenburger DA, Hemann MT. A mammalian functional-genetic approach to characterizing cancer therapeutics. (2011) Nature Chemical Biology. 7(2):92-100.
    13. Reinhardt HC#, Jiang H#, Hemann MT and Yaffe MB. Exploiting synthetic lethal interactions for targeted cancer therapy. (2009) Cell Cycle 8(19) :3112-9. (#equal contribution)
    14. Jiang H#, Reinhardt HC#, Bartkova J, Tommiska J, Blomqvist C, Nevanlinna H, Bartek J, Yaffe MB, Hemann MT. The combined status of ATM and p53 link tumor development with therapeutic response. (2009) Genes & Development. 23(16):1895-909. (#equal contribution)
    15. Jiang H#, Wu J#, He C, Yang W, Li H. Tumor suppressor protein C53 antagonizes checkpoint kinases to promote cyclin-dependent kinase 1 activation. (2009) Cell Research. 19(4):458-68. (#equal contribution)
    16. Jiang H, Luo S, Li H. Cdk5 activator-binding protein C53 regulates apoptosis induced by genotoxic stress via modulating the G2/M DNA damage checkpoint. (2005) Journal of Biological Chemistry. 280(21):20651-9
    获奖及荣誉:
    研究组成员:
  • 合影