<sub id="7xzf7"></sub>

            <thead id="7xzf7"></thead>
            <address id="7xzf7"></address>

              ENGLISH | 院長信箱 | 書記信箱
              師資隊伍
              梁凱威

              1、職稱職務:教授、博士生導師
              2、學科專業: 病理與病理生理學
              3、研究方向: 血液腫瘤、基因轉錄、表觀遺傳
              4、實驗室位置: 基礎醫學院3號樓4樓
              5、Email: kwliang@whu.edu.cn


              6、學習經歷:

              2003-2007 武漢大學,生物學基地班,學士

              2007-2009 武漢大學生命科學學院,生物化學與分子生物學,碩士

              2012-2016 美國Stowers醫學研究所,博士


              7、主要工作經歷與任職
              2011.6-2015.2 美國Stowers醫學研究所, Predoctoral Researcher

              2015.3-2018.3 美國西北大學Feinberg醫學院,Research Associate (博士后)

              2018.5-2018.10 美國西北大學Feinberg醫學院,訪問學者

              2018.3-至今 武漢大學基礎醫學院,教授


              8、目前主要科學研究領域和興趣
                   研究遺傳變異所導致的造血干細胞的惡性轉化為白血病的發病機制,探索和鑒定全新的分子治療靶標和靶向治療策略。前期利用MLL染色體異位所導致的混合系白血病為疾病模型,取得了以下主要成果:(1)發現了炎性信號通路介導野生型MLL泛素化降解的分子機制,揭示了穩定野生型MLL可以靶向混合系白血病中MLL融合蛋白和SEC的轉錄依賴,提出了穩定野生型MLL蛋白作為治療混合系白血病的新策略(Cell, 2017);(2)首次研發了SEC抑制劑KL-1和KL-2, 發現它們抑制SEC介導的轉錄延伸和轉錄成癮,是腫瘤轉錄成癮的全新靶向治療藥物(Cell,2018);(3)系統研究了轉錄輔助因子和激酶參與轉錄調控的具體機制以及其異常在白血病和腫瘤中的功能(Molecular Cell, 2015; MCB, 2015; JBC, 2010; Genes Dev,2012 & 2017; Cancer Cell,2018)。

              課題組的具體方向包括:1. 遺傳變異所導致的白血病的發病機制和靶向治療;2. 腫瘤中的轉錄成癮機制和新靶標鑒定;3. 表觀遺傳變異在白血病發病和轉錄成癮中的功能。

              9、教學情況:
              2017 Chromatin, Epigenetics and Gene Expression, 冷泉港實驗室

              2013 Eukaryotic Gene Expression Course, 冷泉港實驗室


              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.

              專利申請:

              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


              江苏快三软件