黄佳良 HUANG Jialiang, Ph.D.
教授，博士生导师
闽江********
生物信息学与表观基因组学（Bioinformatics and Epigenomics）
课题组长
邮箱：jhuang@xmu.edu.cn
实验室主页：https://huanglab.xmu.edu.cn/
2005年，福州大学，生物工程学士
2008年，福州大学，计算机软件与理论硕士
2012年，中国科学院遗传与发育生物学研究所，生物信息学博士
2011-2013，葛兰素史克上海医药研发有限公司，科学家
2013-2018，哈佛大学Dana-Farber癌症研究所/波士顿儿童医院，博士后
2018年至今，厦门大学生命科学学院，闽江********
2005, B.Sc., Fuzhou University
2008, M.Sc., Fuzhou University
2012, Ph.D., Chinese Academy of Science
2011-2013, Scientist, GlaxoSmithKline (China) R&D Co., Ltd., Shanghai
2013-2018, Postdoc, Dana-Farber Cancer Institute/Boston Children's Hospital, Harvard Medical School
2018-present, Principal Investigator, School of Life Sciences, Xiamen University


研究领域（Research Area）
本课题组利用生物信息学（干）和分子生物学（湿）等方法，研究哺乳动物发育和癌症的表观遗传调控机制。围绕某一特定生物学问题，基于现有/产生表观基因组学等图谱，利用生物信息学方法在系统层面提出具体的生物学假设，并采用CRISPR/cas9基因编辑等手段开展实验验证。具体研究方向包括（1）设计生物信息学算法，解决生物组学数据分析的定量问题；（2）整合已有表观基因组学数据，构建发育过程中的增强子动态调控网络，寻找关键调控因子；（3）与临床医生/生物学家合作，利用单细胞组学等技术，探索癌症发生和治疗的细胞异质性，寻找潜在药物靶标。

Our lab is interest in understanding the epigenetic regulation mechanisms of mammalian development and cancer using computational (dry) and experimental (wet) methods. Starting from a specific biological question, we generate or integrate publicly available genomic and epigenomic data to make a specific testable hypothesis at system level, following by the experimental validation using CRISPR/cas9 genome-editing assays. Our current research includes: (1) developing computational methods for quantification problems for various omics data; (2) elucidate the gene regulatory networks during development through integrating genomic, transcriptomic, and epigenomic data; (3) investigate the cellular heterogeneity during cancer progression and treatment response using single-cell analysis, which helps to identify potential drug targets.
本课题组热诚欢迎具有分子生物学、数理统计和计算机编程等交叉学科基础的硕士生、博士生、博士后和助理教授加盟！




代表性论文（Selected Publications）

1.W. Cai^#, J. Huang^#, Q. Zhu, B. Li, D. Seruggia, P. Zhou, M. Nguyen, Y. Fujiwara, H. Xie, Z. Yang, D. Hong, P. Ren, J. Xu, W. Pu, G.-C. Yuan* and S. H. Orkin*. Enhancer-dependence of cell-type-specific gene expression increases with developmental age. PNAS, 2020; 117: 35.
2.J. Huang^#, K. Li^#, W. Cai, X. Liu, Y. Zhang, S. H. Orkin, J. Xu*, G.-C. Yuan*. Dissecting super-enhancer hierarchy based on chromatin interactions. Nature Communications, 2018; 9:943.
3.J. Huang^#, X. Liu^#, D. Li^#, Z. Shao^#, H. Cao, Y. Zhang, E. Trompouki, T. V. Bowman, L. I. Zon, G.-C. Yuan, S. H. Orkin*, J. Xu*. Dynamic control of enhancer repertoires drives lineage and stage-specific transcription during hematopoiesis. Developmental Cell, 2016; 36, 9-23.
4.J. Huang, E. Marco, L. Pinello, G.-C. Yuan*. Predicting chromatin organization using histone marks. Genome Biology, 2015; 16, 162.
5.J. Huang, C. Niu, C. D.Green, L. Yang, H. Mei*, J.-D. J. Han*. Systematic prediction of pharmacodynamic drug-drug interactions through protein-protein-interaction network. PLoS Computational Biology, 2013; 9, e**.
6.J. Huang, Y. Liu, W. Zhang, H. Yu and J.-D. J. Han*. eResponseNet: a package prioritizing candidate disease genes through cellular pathways. Bioinformatics, 2011; 27, 2319-2320.
7.E. Marco^#, W. Meuleman^#, J. Huang^#, K. Glass, L. Pinello, J. Wang, M. Kellis*, G.-C. Yuan*. Multi-scale chromatin state annotation using a hierarchical hidden Markov model. Nature Communications, 2017; 8, 15011.

8.S. Beyaz^#, J. Kim^#, L. Pinello^#, Y. Hu, M. A. Kerenyi, P. P. Das, R. A. Barnitz, M. E. Xifaras, R. Dogum, J. Huang, W. N. Haining, O. Yilmaz, G.-C. Yuan, S. H. Orkin*, F. Winau*. The histone demethylase UTX regulates the lineage-specific epigenetic program of invariant natural killer T cells. Nature Immunology. 2017; 18, 184-195.
9.H. Xie, C. Peng, J. Huang, B. Li, W. Kim, E. Smith, Y. Fujiwara, J. Qi, G. Cheloni, P. P. Das, M. Nguyen, S. Li, J. E. Bradner, S. H. Orkin*. Chronic myelogenous leukemia initiating cells require Polycomb group protein EZH2. Cancer Discovery, 2016; 6, 1237-1247.
10.S. Luc, J. Huang, J. McEldoon, E. Somuncular, D. Li, C. Rhodes, S. Mamoor, S. Hou, J. Xu, S. H. Orkin*. Bcl11a-deficiency causes hematopoietic stem cell defects with an aging-like phenotype. Cell Reports, 2016; 16, 3181-3194.
11.J. Xu^#, Z. Shao^#, D. Li, H. Xie, W. Kim, J. Huang, J. E. Taylor, L. Pinello, K. Glass, J. D. Jaffe, G.-C. Yuan, S. H. Orkin*. Developmental control of polycomb subunit composition by GATA factors mediates a switch to non-canonical functions. Molecular Cell, 2015; 57, 304-316.