ENGLISH | 院长信箱 | 书记信箱
师资队伍
梁凯威

1、职称职务:教授、博士生导师、国家第十四批千人计划青年项目获得者 
2、学科专业: 病理与病理生理学
3、研究方向: 血液肿瘤、基因转录、表观遗传
4、联系电话:
5Email: 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
2011.6-2015.2 美国Stowers医学研究所, Predoctoral Researcher

2015.3-2018.3 美国西北大学Feinberg医学院,Research Associate (博士后)

2018.5-2018.10 美国西北大学Feinberg医学院,访问学者

2018.3-至今 武汉大学基础医学院,教授


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染色体异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; JBC, 2010; Genes Dev,2012 & 2017; Cancer Cell,2018)。

课题组的具体方向包括:1. 遗传变异所导致的白血病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. 表观遗传变异在白血病发病和转录成瘾中的功能。

9、教学情况:
2017 Chromatin, Epigenetics and Gene Expression, 冷泉港实验室

2013 Eukaryotic Gene Expression Course, 冷泉港实验室


10、代表性成果

1. 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 Through SEC Disruption. Cell, 2018 (In press).

2. 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(Accepted)

3. 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. (Previewed by NEJM)

4. L. Wang, C. K. Collings, Z. Zhao, K. A. Cozzolino, Q. Ma, K. Liang, S. A. Marshall, C. C. Sze, R. Hashizume, J. N. Savas, and A. Shilatifard, A Cytoplasmic Compass Is Necessary for Cell Survival and Triple-Negative Breast Cancer Pathogenesis by Regulating Metabolism. Genes Dev, 2017. 31(20): p. 2056-2066.

5. C. C. Ebmeier, B. Erickson, B. L. Allen, M. A. Allen, H. Kim, N. Fong, J. R. Jacobsen, K. Liang, A. Shilatifard, R. D. Dowell, W. M. Old, D. L. Bentley, and D. J. Taatjes, Human Tfiih Kinase Cdk7 Regulates Transcription-Associated Chromatin Modifications. Cell Rep, 2017. 20(5): p. 1173-1186.

6. 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. (封面文章)

7. 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.

8. H. M. Herz, M. Mohan, A. S. Garruss, K. Liang, Y. H. Takahashi, K. Mickey, O. Voets, C. P. Verrijzer, and A. Shilatifard, Enhancer-Associated H3k4 Monomethylation by Trithorax-Related, the Drosophila Homolog of Mammalian Mll3/Mll4. Genes Dev, 2012. 26(23): p. 2604-20.

9. 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.

专利申请:

1. A .Shilatifard, K. Liang and E.R. Smith, Therapeutic Targeting Of Interleukin-1 Receptor-Associated Kinase 4 (Irak4) In Cancers Characterized By Rearrangements In The Mixed Lineage Leukemia Gene (MLL-R) Serial No.15/497,783

2. A. Shilatifard, K.Liang, E. R Smith, and G. E. Schiltz, Small Molecules for Disrupting the Super Elongation Complex and Inhibiting Transcription Elongation for Cancer Therapy, Serial No.  62/645,890