1、职称职务：教授、博士生导师

2、学科专业：生理学

3、研究方向：基因转录、表观遗传、血液肿瘤

4、实验室位置：基础医学院3号楼4楼

5、Email： kwliang@whu.edu.cn

6、学习经历：

2003-2007 武汉大学，生物学基地班，学士

2007-2009 武汉大学生命科学学院，生物化学与分子生物学，硕士

2012-2016 美国Stowers医学研究所，博士

7、主要工作经历与任职

2011.06–2011.12  美国Stowers医学研究所, Predoctoral Researcher

2012.01–2016.05  美国Stowers医学研究所博士研究生

2016.07–2018.03  美国西北大学Feinberg医学院博士后

2018.03–至今        武汉大学基础医学院教授（其间：2018.05–2018.10美国西北大学Feinberg医学院访问学者）

8、目前主要科学研究领域和兴趣

     研究遗传变异所导致的造血干细胞的恶性转化为白血病的发病机制，探索和鉴定全新的分子治疗靶标和靶向治疗策略。前期利用MLL染色体易位所导致的混合系白血病为疾病模型，取得了以下主要成果：(1)发现了炎性信号通路介导野生型MLL泛素化降解的分子机制，揭示了稳定野生型MLL可以靶向混合系白血病中MLL融合蛋白和SEC的转录依赖，提出了稳定野生型MLL蛋白作为治疗混合系白血病的新策略（Cell, 2017）；(2)首次研发了SEC抑制剂KL-1和KL-2, 发现它们抑制SEC介导的转录延伸和转录成瘾，是肿瘤转录成瘾的全新靶向治疗药物（Cell，2018）；(3)系统研究了转录辅助因子和激酶参与转录调控的具体机制以及其异常在白血病和肿瘤中的功能（Molecular Cell, 2015; MCB, 2015; Genes Dev，2012 & 2017； Cancer Cell，2018）。

课题组研究方向包括：1. 遗传变异和表观遗传变异所导致的血液肿瘤的发病机制和靶向治疗;2. 肿瘤中的转录成瘾机制和新靶标鉴定; 3.基于转录成瘾机制的小分子靶向药物开发。

9、教学情况：

本科生课程：“生理学”，“病理生理学”，“损伤与反应”，“生物医学技术前沿”， “医学与健康”

2017 Chromatin, Epigenetics and Gene Expression, 冷泉港实验室

2013 Eukaryotic Gene Expression Course, 冷泉港实验室

10、获批资助项目

科技部“干细胞与转化”重点研发计划青年项目

湖北省医学青年第一层次资助

武汉大学人才引进项目

11、近期代表性论文

Wang K#, Wang H#, Li C#, Yin Z, Xiao R, Li Q, Xiang Y, Wang W, Huang J, Chen L, Fang P*, Liang K*. Genomic Profiling of Native R-loops with a DNA-RNA Hybrid Recognition Sensor. Science Advances 2021(in press)

J. Wu#, J. Yan#, P. Fang, H.B. Zhou, K. Liang *, and J. Huang* (2019). Three-dimensional oxabicycloheptene sulfonate targets the homologous recombination and repair programmes through estrogen receptor alpha antagonism. Cancer Lett 469, 78-88.

R. Xiao#, H.Wang#, and K. Liang*, Transcriptional Addiction in Mixed Lineage Leukemia: New Avenues for Target Therapies. Blood Science, 2019. 1: p.50-56.

K. Liang, E. R. Smith, Y. Aoi, K. L. Stoltz, H. Katagi, A. R. Woodfin, E. J. Rendleman, S. A. Marshall, D. C. Murray, L.Wang, P. A. Ozark, R.K. Mishra, R. Hashizume, G. E. Schiltz, and A. Shilatifard, Targeting Processive Transcription Elongation Via SEC Disruption For MYC-induced Cancer Therapy. Cell, 2018. 175(3) p. 766-779 e17. (Highlighted by Cancer Discovery and Nature Reviews Cancer)

A. Volk, K. Liang, J. Zhao, X. Li, M.Bulic, S. Marshall, J.W. Taub, Y. Ge, S. Malinge, E. Bartom, A. Shilatifard, and J.D Crispino, A CHAF1B-Dependent Molecular Switch in Hematopoiesis and Leukemic Pathogenesis. Cancer Cell, 2018. 34: p. 707-724. (Previewed by Cancer Cell)

K. Liang, A. G. Volk, J. S. Haug, S. A. Marshall, A. R. Woodfin, E. T. Bartom, J. M. Gilmore, L. Florens, M. P. Washburn, K. D. Sullivan, J. M. Espinosa, J. Cannova, J. Zhang, E. R. Smith, J. D. Crispino, and A. Shilatifard, Therapeutic Targeting of Mll Degradation Pathways in Mll-Rearranged Leukemia. Cell, 2017. 168(1-2): p. 59-72 e13. (Highlighted by Cancer Discovery and Science Translational Medicine, recommended by Faculty of 1000 Prime, Previewed by NEJM)

K. Liang, A. R. Woodfin, B. D. Slaughter, J. R. Unruh, A. C. Box, R. A. Rickels, X. Gao, J. S. Haug, S. L. Jaspersen, and A. Shilatifard, Mitotic Transcriptional Activation: Clearance of Actively Engaged Pol Ii Via Transcriptional Elongation Control in Mitosis. Mol Cell, 2015. 60(3): p. 435-45. (Selected for the cover)

K. Liang, X. Gao, J. M. Gilmore, L. Florens, M. P. Washburn, E. Smith, and A. Shilatifard, Characterization of Human Cyclin-Dependent Kinase 12 (Cdk12) and Cdk13 Complexes in C-Terminal Domain Phosphorylation, Gene Transcription, and Rna Processing. Mol Cell Biol, 2015. 35(6): p. 928-38. (Highlighted by MCB)

K. Liang#, L. Yang#, C. Yin, Z. Xiao, J. Zhang, Y. Liu, and J. Huang, Estrogen Stimulates Degradation of Beta-Amyloid Peptide by up-Regulating Neprilysin. J Biol Chem, 2010. 285(2): p. 935-42. (Highlighted by JBC)

Zheng, H#., Qi, Y#., Hu, S#., Cao, X#., Xu, C#., Yin, Z., Chen, X., Li, Y., Liu, W., Li, J., et al. (2020). Identification of Integrator-PP2A complex (INTAC), an RNA polymerase II phosphatase. Science 370.

Cao, K., Ugarenko, M., Ozark, P.A., Wang, J., Marshall, S.A., Rendleman, E.J., Liang, K., Wang, L., Zou, L., Smith, E.R., et al. (2020). DOT1L-controlled cell-fate determination and transcription elongation are independent of H3K79 methylation. Proc Natl Acad Sci U S A 117, 27365-27373.

Wang, L., Collings, C.K., Zhao, Z., Cozzolino, K.A., Ma, Q., Liang, K., Marshall, S.A., Sze, C.C., Hashizume, R., Savas, J.N., et al. (2017). A cytoplasmic COMPASS is necessary for cell survival and triple-negative breast cancer pathogenesis by regulating metabolism. Genes Dev 31, 2056-2066.

Ebmeier, C.C., Erickson, B., Allen, B.L., Allen, M.A., Kim, H., Fong, N., Jacobsen, J.R., Liang, K., Shilatifard, A., Dowell, R.D., et al. (2017). Human TFIIH Kinase CDK7 Regulates Transcription-Associated Chromatin Modifications. Cell Rep 20, 1173-1186.

Herz, H.M., Mohan, M., Garruss, A.S., Liang, K., Takahashi, Y.H., Mickey, K., Voets, O., Verrijzer, C.P., and Shilatifard, A. (2012). Enhancer-associated H3K4 monomethylation by Trithorax-related, the Drosophila homolog of mammalian Mll3/Mll4. Genes Dev 26, 2604-2620.

12、专利申请：

Ali Shilatifard, Kaiwei Liang, and Edwin Richard Smith, Therapeutic Targeting of Interleukin-1 Receptor-Associated Kinase 4 (Irak4) in Cancers Characterized by Rearrangements in the Mixed Lineage Leukemia Gene (Mll-R). 2017, US Patent App. 15/497,783. Approved

Ali Shilatifard, Kaiwei Liang, Edwin Richard, Smith, Gary E. Schiltz, Small Molecules for Disrupting the Super Elongation Complex and Inhibiting Transcription Elongation for Cancer Therapy. U.S. Serial No: 62/645,890 Filing Date: March 21, 2018 pending

欢迎有志于从事表观遗传学和肿瘤靶向治疗研究的优秀学生报考！